https://orcid.org/0000-0001-8394-0150
Peer Review History
| Original SubmissionJanuary 24, 2026 |
|---|
|
-->PONE-D-26-03912-->-->Dietary cholesterol reduces blood pressure and alters lipid profiles in stroke-prone spontaneously hypertensive rats-->-->PLOS One Dear Dr. Tatematsu, Thank you for submitting your manuscript to PLOS ONE. After careful consideration, we feel that it has merit but does not fully meet PLOS ONE’s publication criteria as it currently stands. Therefore, we invite you to submit a revised version of the manuscript that addresses the points raised during the review process. Please submit your revised manuscript by Apr 19 2026 11:59PM. If you will need more time than this to complete your revisions, please reply to this message or contact the journal office at plosone@plos.org. When you're ready to submit your revision, log on to https://www.editorialmanager.com/pone/ and select the 'Submissions Needing Revision' folder to locate your manuscript file. Please include the following items when submitting your revised manuscript:-->
If you would like to make changes to your financial disclosure, please include your updated statement in your cover letter. Guidelines for resubmitting your figure files are available below the reviewer comments at the end of this letter. If applicable, we recommend that you deposit your laboratory protocols in protocols.io to enhance the reproducibility of your results. Protocols.io assigns your protocol its own identifier (DOI) so that it can be cited independently in the future. For instructions see: https://journals.plos.org/plosone/s/submission-guidelines#loc-laboratory-protocols. Additionally, PLOS ONE offers an option for publishing peer-reviewed Lab Protocol articles, which describe protocols hosted on protocols.io. Read more information on sharing protocols at https://plos.org/protocols?utm_medium=editorial-email&utm_source=authorletters&utm_campaign=protocols. We look forward to receiving your revised manuscript. Kind regards, Luis Eduardo M Quintas, Ph.D. Academic Editor PLOS One Journal Requirements: When submitting your revision, we need you to address these additional requirements. 1. Please ensure that your manuscript meets PLOS ONE's style requirements, including those for file naming. The PLOS ONE style templates can be found at https://journals.plos.org/plosone/s/file?id=wjVg/PLOSOne_formatting_sample_main_body.pdf and 2. We note that the grant information you provided in the ‘Funding Information’ and ‘Financial Disclosure’ sections do not match. When you resubmit, please ensure that you provide the correct grant numbers for the awards you received for your study in the ‘Funding Information’ section. 3. Thank you for stating the following financial disclosure: “This work was supported by JSPS KAKENHI Grant Numbers JP22K05526.” Please state what role the funders took in the study. If the funders had no role, please state: "The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript." If this statement is not correct you must amend it as needed. Please include this amended Role of Funder statement in your cover letter; we will change the online submission form on your behalf. 4. When completing the data availability statement of the submission form, you indicated that you will make your data available on acceptance. We strongly recommend all authors decide on a data sharing plan before acceptance, as the process can be lengthy and hold up publication timelines. Please note that, though access restrictions are acceptable now, your entire data will need to be made freely accessible if your manuscript is accepted for publication. This policy applies to all data except where public deposition would breach compliance with the protocol approved by your research ethics board. If you are unable to adhere to our open data policy, please kindly revise your statement to explain your reasoning and we will seek the editor's input on an exemption. Please be assured that, once you have provided your new statement, the assessment of your exemption will not hold up the peer review process. 5. If the reviewer comments include a recommendation to cite specific previously published works, please review and evaluate these publications to determine whether they are relevant and should be cited. There is no requirement to cite these works unless the editor has indicated otherwise. [Note: HTML markup is below. Please do not edit.] Reviewers' comments: Reviewer's Responses to Questions -->Comments to the Author 1. Is the manuscript technically sound, and do the data support the conclusions? The manuscript must describe a technically sound piece of scientific research with data that supports the conclusions. Experiments must have been conducted rigorously, with appropriate controls, replication, and sample sizes. The conclusions must be drawn appropriately based on the data presented. --> Reviewer #1: Yes ********** -->2. Has the statistical analysis been performed appropriately and rigorously? --> Reviewer #1: Yes ********** -->3. Have the authors made all data underlying the findings in their manuscript fully available? The PLOS Data policy requires authors to make all data underlying the findings described in their manuscript fully available without restriction, with rare exception (please refer to the Data Availability Statement in the manuscript PDF file). The data should be provided as part of the manuscript or its supporting information, or deposited to a public repository. For example, in addition to summary statistics, the data points behind means, medians and variance measures should be available. If there are restrictions on publicly sharing data—e.g. participant privacy or use of data from a third party—those must be specified.--> Reviewer #1: Yes ********** -->4. Is the manuscript presented in an intelligible fashion and written in standard English? PLOS ONE does not copyedit accepted manuscripts, so the language in submitted articles must be clear, correct, and unambiguous. Any typographical or grammatical errors should be corrected at revision, so please note any specific errors here.--> Reviewer #1: Yes ********** -->5. Review Comments to the Author Please use the space provided to explain your answers to the questions above. You may also include additional comments for the author, including concerns about dual publication, research ethics, or publication ethics. (Please upload your review as an attachment if it exceeds 20,000 characters)--> Reviewer #1: Dear Editor of PLOS ONE, Thank you for the opportunity to review manuscript PONE-D-26-03912, entitled “Dietary cholesterol reduces blood pressure and alters lipid profiles in stroke-prone spontaneously hypertensive rats.” The study contributes to a relevant discussion in nutrition and vascular pathophysiology by examining, in an experimental model of severe hypertension and hemorrhagic stroke, the apparent paradox between the traditionally assigned role of dietary cholesterol as a cardiovascular risk factor and prior evidence of increased survival in SHRSP animals fed a cholesterol-enriched diet. Methodologically, the authors randomized male SHRSP/Izm rats (4 weeks old; n = 6/group) to three dietary conditions for 12 weeks: a control diet, a diet containing 1% (w/w) cholesterol, and a diet containing 1% cholesterol plus 0.025% (w/w) lovastatin (to suppress endogenous synthesis). They assessed pre/post systolic blood pressure and performed integrated analyses of sterols (including phytosterols), fatty acid composition, PGE₂ levels, and renal histopathology. As the main findings, the cholesterol group exhibited a significant ~9–10% reduction in systolic blood pressure, accompanied by marked changes in the lipid profile, including modulation of phytosterols and a reduction in the arachidonic acid ratio in serum and kidney. In addition, the authors report a trend toward decreased PGE₂ and a modest attenuation of renal alterations. The authors interpret these results as evidence that dietary cholesterol may reduce renal phytosterol accumulation and suppress the AA–PGE₂ axis, potentially linking biochemical changes to improved renal/inflammatory status and to the phenotype previously associated with increased survival in this model. Overall, I recommend a Major Revision. While the dataset is potentially suitable for publication in PLOS ONE, several issues should be addressed to ensure that the conclusions remain proportional to the evidence presented. In particular, sections of the Discussion and Conclusions repeatedly imply reduced hemorrhagic stroke risk and/or lifespan extension, yet survival and stroke incidence were not directly measured in the current study; these statements should be reframed as hypotheses grounded in prior reports and tied more explicitly to the measured endpoints (e.g., SBP changes, lipid profile shifts, and renal histology). In addition, there are internal consistency and reporting issues that require correction and greater transparency—most notably, a discrepancy regarding the direction of Ldlr expression in the statin group (as described in different sections), incomplete specification of statistical procedures (including distributional checks and handling of potential outliers), and figure presentation that would benefit from displaying individual data points given the small group sizes (n = 6). Addressing these points, along with careful moderation of mechanistic claims (e.g., inflammatory pathway activation inferred from mRNA and limited mediator measurements), would substantially strengthen the manuscript. Minor/editorial comments Introduction L49–L51: The phrase “animal fats and oils” reads slightly imprecise (oils are typically plant-derived). Consider “animal-sourced foods” / “animal-derived foods,” depending on what you intend to emphasize. L51–L52: “blood Chol” is broad. If you are referring to clinical/epidemiological evidence, please specify the metric (e.g., total cholesterol vs LDL-C), as this affects interpretation. L52–L54: Consider replacing “widely acknowledged” with “well-established” to keep the tone neutral and improve readability. L52–L54: The plaque sentence could be streamlined. For instance, instead of “primarily due to the propensity for the formation…,” consider a more direct construction such as: “because it promotes the development of cholesterol-rich plaques.” L54–L56: In epidemiological writing, “inverse association” is often preferred over “inverse correlation” unless a correlation coefficient is being reported. L59: There is a clear line-break/formatting issue (“…established as 59 a model…”). Please correct to ensure the sentence reads smoothly. L60–L61: Consider tightening for flow and precision. For example: “In this strain, lifespan is curtailed by fatal strokes secondary to severe hypertension and renal impairment.” L62 (abbreviation clarity—important): In lipid nomenclature, “PS” is widely used for phosphatidylserine. Because you use “PS” to mean phytosterols, I strongly recommend avoiding the abbreviation “PS” throughout the manuscript. Options: write “phytosterols” in full, or define an alternative (e.g., PhyS or plant sterols (PLS)). At minimum, add a note at first use (e.g., “phytosterols, hereafter abbreviated as PhyS to avoid confusion with phosphatidylserine”). L62–L63: “shorten survival” (or “reduce survival”) is more idiomatic than “shorten the survival.” Also, “by increasing blood pressure” can be simplified to “by raising blood pressure.” L62–L63: Since phytosterols are central to the paradox, consider briefly specifying whether the effect is attributed to phytosterols generally or to specific sterols (e.g., sitosterol/campesterol), depending on what the cited work supports. L64–L66: The ABCG5 statement would benefit from a bit more specificity for a general readership: is the mutation functionally described as loss-of-function with impaired sterol efflux? Also, “target tissues” is vague—if supported by the cited literature, consider naming the most relevant tissues (e.g., kidney/vasculature/brain). L66–L67: For readability, consider simplifying the causal chain. Example: “Accumulated phytosterols can partially replace membrane cholesterol, which may reduce membrane integrity and increase vascular fragility [10].” L68–L69: Unless the cited work directly demonstrates rupture causality, consider a more cautious phrasing: “may predispose cerebral vessels to rupture, contributing to hemorrhagic stroke.” L81: “blood pressure elevation [15–17]” appears as a sentence fragment (possibly due to formatting). Please revise so it connects grammatically to its subject/verb. L81–L83 (abbreviation): “Stt” is not a standard abbreviation and is unclear at first read. If you mean statins, I suggest writing “statins” throughout (or use “lovastatin treatment” / “statin treatment” rather than “Stt”). L82–L83: Consider tightening wording and making sure it reflects what the cited studies actually measured (survival vs stroke incidence/severity vs surrogate outcomes). L83: “excessive dietary Chol intake” is subjective. Consider replacing with a concrete phrasing such as “a cholesterol-enriched diet” and/or specify the % (w/w) used. L85–L86: Formatting issue in “sterol regulatory element86 binding proteins.” Please correct to “sterol regulatory element–binding proteins (SREBPs).” L85–L86: Consider specifying which SREBP is most relevant here (SREBP-1 vs SREBP-2), depending on whether the focus is FA synthesis vs cholesterol homeostasis. L87–L88: “have been identified as playing pivotal roles” can be simplified to a more neutral phrasing (e.g., “PUFAs… play key roles in inflammatory regulation”). L88–L90: When introducing AA from PGs, you may optionally acknowledge AA also feeds other eicosanoid classes (TX/LT), but keeping it focused on PGE₂ is also reasonable if that is the main readout. L90–L91: The bridge “Therefore, alterations in sterol composition may influence FA-derived inflammatory pathways” is important. Consider adding one short mechanistic clause (membrane remodeling, substrate availability, enzyme regulation) to make the link less implicit. L91–L94: “remain to be elucidated” appears twice in close succession. Consider rephrasing one instance to “remain unclear” or splitting into shorter sentences. L94–L97: Please avoid “Stt” unless clearly defined and used consistently. Also, because “PS” is commonly phosphatidylserine, I recommend the phytosterol abbreviation fix here as well. L95–L97: “these interactions induce pathologies” is stronger than needed; consider “may contribute to disease-relevant pathways/phenotypes.” Likewise, “offers significant insights” could be toned down to “may provide insight” for a balanced tone. Materials and Methods L105–L106: Please provide a brief description of the basal diet (5001) macronutrient profile (or cite the datasheet), since background fat/sterol content can influence lipid outcomes. Also clarify whether 5001 was meal vs pelleted during feeding. L106–L110: “Stt group” remains unclear/atypical. If this group is specifically Chol + lovastatin, consider renaming to “Chol+Lovastatin” (or “Chol+Statin”) and define it once. L108–L110: For reproducibility, please describe how cholesterol and lovastatin were incorporated (powder vs solvent), mixing equipment/time, whether homogeneity was assessed, and whether diets were fed as meal or re-pelleted. L112: “compositions of fatty FA and sterol contents” appears to be a typo. Suggest “fatty acid composition and sterol content.” L207–L211: Please report whether normality (e.g., Shapiro–Wilk) and homogeneity of variances (e.g., Levene or Brown–Forsythe) were assessed before one-way ANOVA, and what was done if assumptions were violated. L207–L211: Please clarify whether any outlier screening was performed (and which method), including pre-specified criteria and whether exclusions occurred. If none, a brief statement would improve transparency. Results Figures: With n = 6/group, I recommend plotting individual data points overlaid on bars/means (or switching to dot/box plots). Please ensure legends state exact n, whether n refers to animals vs cages (food intake), and whether error bars are SD vs SEM. Where helpful (especially with small n), please consider also reporting the range (min–max) for key endpoints—either in figure legends, supplementary tables, or the Results text. This would make variability and group overlap easier to interpret alongside mean ± SD. L216–L217: “throughout the 12-week feeding period” implies a repeated-measures analysis. If only endpoints were compared, please rephrase accordingly; if time-course statistics were used, specify the model. L218: Typo: “ecrease” → “decrease.” L220–L222 / Table 4: Please report organ weights normalized to body weight (e.g., liver/body weight ratio) and include body weight at sacrifice. Table 4 (scope/rationale): Given this is a severe hypertension/stroke model, it would be helpful to clarify the rationale for the organ panel. If available, reporting heart, brain, and adipose tissue weights (absolute + normalized) could add interpretive value; if not collected, a brief justification would help. L241–L242: Please specify whether sterols/FAs are reported as absolute concentrations (e.g., mg/g tissue; µg/mL serum) or relative composition (%). This affects how “increase/decrease” should be interpreted. L243–L246: Please state key comparisons consistently (Ctr vs Chol vs Stt), then add Chol vs Stt where relevant. This will read more cleanly. L246–L248: Grammar issue (“In relation to PS, resulted…”). Please revise and also remind the reader what the abbreviation refers to—ideally avoid “PS” given the phosphatidylserine conflict. L247–L251: The phytosterol redistribution pattern is interesting (increase hepatic campesterol/total phytosterols; decrease serum and kidney). Consider adding one short mechanistic sentence (even if cautious) linking this to known transport/excretion pathways, or explicitly state that the mechanism remains unclear. L249–L251: “β-sitosterol decreased across all tissues” should clarify whether this is absolute concentration or proportional composition (important given total phytosterols change in different directions by tissue). L260–L267: Please clarify “total FA level” (absolute amount) vs “composition” (%). The AA decrease across tissues is a key observation; consider a short mechanistic hypothesis (LA→AA flux vs remodeling/Lands’ cycle), especially since AA decreases in Chol even when Fads1/2 do not change. L264–L265: Define “kidney PL” operationally (phospholipid fraction). If liver/serum reflect different fractions, please make that explicit so readers compare appropriately. Fig 4 / L287–L289: Please specify PGE₂ units and method (ELISA vs LC-MS/MS; normalization), and align wording with significance (liver significant vs kidney trend). Exact p-values would help. Fig 5 / SOD: Please clarify how SOD activity was measured and normalized (tissue per mg protein; serum per mL; hemolysis checks). Also specify which statistical test was used for SOD (Methods currently notes it differed, but does not state how). qPCR: Please ensure Methods/legends report housekeeping gene(s), ΔΔCt approach, primer sequences/efficiencies, biological and technical replicates, and how fold-changes are plotted (linear vs log). L313–L320: Npc1l1 is often discussed in intestinal absorption; if hepatic Npc1l1 is central here, add a brief justification/citation. Also, the Ldlr description should explicitly indicate which pairwise comparisons are statistically significant (avoid qualitative terms without stats). L337–L340: It would strengthen Results to explicitly connect increased Srebf1c/Scd1 in Chol to the MUFA shifts (Tables 5–6), even in one sentence. Fig 6C vs Fig 4: You report increased Cox-2/Ep3/Ep4 mRNA in Chol while hepatic PGE₂ is decreased. This is not necessarily contradictory, but it deserves one brief clarifying sentence (e.g., substrate limitation due to AA reduction, post-transcriptional regulation, activity vs transcript). Histology (Fig 7 / Table 8): Please clarify whether scoring was blinded, provide explicit grade definitions (±, +, etc.), indicate sections/fields examined per animal, and state whether ordinal data were analyzed statistically (or state explicitly if not analyzed due to low frequency). Discussion The Discussion is informative but feels overly long and somewhat repetitive, and several mechanistic chains are described with a level of certainty that goes beyond what was directly measured. I suggest tightening the Discussion by focusing on the primary observed endpoints (SBP, sterol redistribution, AA/PGE₂ patterns, renal histology) and presenting mechanistic links (e.g., LXR/oxysterols/OPS; systemic anti-inflammation; lifespan extension) more explicitly as hypotheses or future directions unless directly supported. Consider adding a simple schematic/graphical summary (either as a main figure) that lays out your proposed working model: dietary cholesterol → changes in phytosterol handling/redistribution (liver vs kidney) + modulation of AA availability and PGE₂ → renal histology/BP phenotype, with the lovastatin arm shown as a modifier. A clear “working model” figure would make the narrative easier to follow and would help distinguish measured outcomes from inferred mechanisms. Key questions for the authors Question 1: In the epidemiological literature cited in the first paragraph, which cholesterol metric (total cholesterol vs LDL-C/HDL-C) and which hemorrhagic stroke subtype (intracerebral vs subarachnoid) are most responsible for the reported inverse association? How should readers think about that human framing relative to the SHRSP model used here? Question 2: To make the “paradox” framing more convincing, could you clarify whether the previously reported lifespan extension on a cholesterol-rich diet reflects an effect of cholesterol per se, or whether broader diet features could have contributed (diet composition, phytosterol handling, or energy intake)? Were these factors monitored in the cited survival studies and/or in the present work?? Question 3: When you mention that “Stt” improves survival in SHRSP rats, do you mean statins as a class or a specific statin/dose? Since this study uses lovastatin, it would help if the Introduction matched the prior evidence (class vs specific compound) more explicitly to the intervention tested here. Question 4: Were the three diets isocaloric and matched for macronutrient/fat content, aside from the added cholesterol and lovastatin? If not, please report energy density and explain how potential intake differences were handled. Question 5: A key point for interpretation: are the AA decreases driven by reductions in absolute AA content, or are they mainly relative (% total FA) shifts due to expansion of other FA pools (e.g., MUFAs and/or 18:2n-6)? A clear statement on concentration vs composition (and the lipid fraction analyzed in each tissue) would help. Question 6: Hepatic PGE₂ decreases while Cox-2 and EP receptor transcripts increase in the Chol group. How do you reconcile this pattern? Is your working model that reduced AA availability limits PGE₂ production despite higher Cox-2 mRNA, or were protein/activity measures considered to support pathway interpretation? Question 7: Given the Abcg5 mutation, do you interpret increased hepatic Abcg5/8 and Npc1l1 mRNA as a compensatory response to sterol accumulation? If so, is there any functional readout (fecal/biliary sterols, protein levels, or another proxy) that supports altered sterol flux beyond transcript changes? Question 8: I may have missed this in the Methods—was histological scoring performed blinded to group allocation, and were ordinal scores analyzed statistically (or explicitly treated as descriptive due to low frequency)? A short clarification here would increase confidence in the renal pathology interpretation. Overall, I find the topic timely and the experimental approach interesting, particularly the attempt to isolate dietary cholesterol effects without changing fatty acid composition. However, several points require clarification and some conclusions should be toned down to better match the endpoints measured (SBP, lipid profiles, PGE₂, and histology, without direct survival/stroke outcomes). Addressing the questions above and improving reporting transparency (diet composition, statistics, and data presentation) would substantially strengthen the manuscript and its interpretability. ********** -->6. PLOS authors have the option to publish the peer review history of their article (what does this mean?). If published, this will include your full peer review and any attached files. If you choose “no”, your identity will remain anonymous but your review may still be made public. Do you want your identity to be public for this peer review? For information about this choice, including consent withdrawal, please see our Privacy Policy.--> Reviewer #1: Yes: Israel Jose Pereira Garcia ********** [NOTE: If reviewer comments were submitted as an attachment file, they will be attached to this email and accessible via the submission site. Please log into your account, locate the manuscript record, and check for the action link "View Attachments". If this link does not appear, there are no attachment files.] To ensure your figures meet our technical requirements, please review our figure guidelines: https://journals.plos.org/plosone/s/figures You may also use PLOS’s free figure tool, NAAS, to help you prepare publication quality figures: https://journals.plos.org/plosone/s/figures#loc-tools-for-figure-preparation. NAAS will assess whether your figures meet our technical requirements by comparing each figure against our figure specifications.
|
| Revision 1 |
|
Dietary cholesterol reduces blood pressure and alters lipid profiles in stroke-prone spontaneously hypertensive rats PONE-D-26-03912R1 Dear Dr. Tatematsu, We’re pleased to inform you that your manuscript has been judged scientifically suitable for publication and will be formally accepted for publication once it meets all outstanding technical requirements. Within one week, you’ll receive an e-mail detailing the required amendments. When these have been addressed, you’ll receive a formal acceptance letter and your manuscript will be scheduled for publication. An invoice will be generated when your article is formally accepted. Please note, if your institution has a publishing partnership with PLOS and your article meets the relevant criteria, all or part of your publication costs will be covered. Please make sure your user information is up-to-date by logging into Editorial Manager at Editorial Manager® and clicking the ‘Update My Information' link at the top of the page. For questions related to billing, please contact billing support. If your institution or institutions have a press office, please notify them about your upcoming paper to help maximize its impact. If they’ll be preparing press materials, please inform our press team as soon as possible -- no later than 48 hours after receiving the formal acceptance. Your manuscript will remain under strict press embargo until 2 pm Eastern Time on the date of publication. For more information, please contact onepress@plos.org. Kind regards, Luis Eduardo M Quintas, Ph.D. Academic Editor PLOS One Additional Editor Comments (optional): Reviewers' comments: Reviewer's Responses to Questions -->Comments to the Author 1. If the authors have adequately addressed your comments raised in a previous round of review and you feel that this manuscript is now acceptable for publication, you may indicate that here to bypass the “Comments to the Author” section, enter your conflict of interest statement in the “Confidential to Editor” section, and submit your "Accept" recommendation.--> Reviewer #1: All comments have been addressed ********** -->2. Is the manuscript technically sound, and do the data support the conclusions? The manuscript must describe a technically sound piece of scientific research with data that supports the conclusions. Experiments must have been conducted rigorously, with appropriate controls, replication, and sample sizes. The conclusions must be drawn appropriately based on the data presented. --> Reviewer #1: Yes ********** -->3. Has the statistical analysis been performed appropriately and rigorously? --> Reviewer #1: Yes ********** -->4. Have the authors made all data underlying the findings in their manuscript fully available? The PLOS Data policy requires authors to make all data underlying the findings described in their manuscript fully available without restriction, with rare exception (please refer to the Data Availability Statement in the manuscript PDF file). The data should be provided as part of the manuscript or its supporting information, or deposited to a public repository. For example, in addition to summary statistics, the data points behind means, medians and variance measures should be available. If there are restrictions on publicly sharing data—e.g. participant privacy or use of data from a third party—those must be specified.--> Reviewer #1: Yes ********** -->5. Is the manuscript presented in an intelligible fashion and written in standard English? PLOS ONE does not copyedit accepted manuscripts, so the language in submitted articles must be clear, correct, and unambiguous. Any typographical or grammatical errors should be corrected at revision, so please note any specific errors here.--> Reviewer #1: Yes ********** -->6. Review Comments to the Author Please use the space provided to explain your answers to the questions above. You may also include additional comments for the author, including concerns about dual publication, research ethics, or publication ethics. (Please upload your review as an attachment if it exceeds 20,000 characters)--> Reviewer #1: (No Response) ********** -->7. PLOS authors have the option to publish the peer review history of their article (what does this mean?). If published, this will include your full peer review and any attached files. If you choose “no”, your identity will remain anonymous but your review may still be made public. Do you want your identity to be public for this peer review? For information about this choice, including consent withdrawal, please see our Privacy Policy.--> Reviewer #1: Yes: Israel Jose Pereira Garcia ********** |
| Formally Accepted |
|
PONE-D-26-03912R1 PLOS One Dear Dr. Tatematsu, I'm pleased to inform you that your manuscript has been deemed suitable for publication in PLOS One. Congratulations! Your manuscript is now being handed over to our production team. At this stage, our production department will prepare your paper for publication. This includes ensuring the following: * All references, tables, and figures are properly cited * All relevant supporting information is included in the manuscript submission, * There are no issues that prevent the paper from being properly typeset You will receive further instructions from the production team, including instructions on how to review your proof when it is ready. Please keep in mind that we are working through a large volume of accepted articles, so please give us a few days to review your paper and let you know the next and final steps. Lastly, if your institution or institutions have a press office, please let them know about your upcoming paper now to help maximize its impact. If they'll be preparing press materials, please inform our press team within the next 48 hours. Your manuscript will remain under strict press embargo until 2 pm Eastern Time on the date of publication. For more information, please contact onepress@plos.org. You will receive an invoice from PLOS for your publication fee after your manuscript has reached the completed accept phase. If you receive an email requesting payment before acceptance or for any other service, this may be a phishing scheme. Learn how to identify phishing emails and protect your accounts at https://explore.plos.org/phishing. If we can help with anything else, please email us at customercare@plos.org. Thank you for submitting your work to PLOS ONE and supporting open access. Kind regards, PLOS ONE Editorial Office Staff on behalf of Dr. Luis Eduardo M Quintas Academic Editor PLOS One |
Open letter on the publication of peer review reports
PLOS recognizes the benefits of transparency in the peer review process. Therefore, we enable the publication of all of the content of peer review and author responses alongside final, published articles. Reviewers remain anonymous, unless they choose to reveal their names.
We encourage other journals to join us in this initiative. We hope that our action inspires the community, including researchers, research funders, and research institutions, to recognize the benefits of published peer review reports for all parts of the research system.
Learn more at ASAPbio .