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COPD: A possible explanation, and treatment

Posted by dwmoskowitz on 20 Mar 2010 at 17:43 GMT

We found (1) that overactivity of angiotensin I-converting enzyme (ACE), i.e. the deletion/deletion (D/D) genotype, was associated with COPD as well as all the diseases mentioned in this article. We also found that inhibiting ACE had a dramatic effect on the progression of even end-stage COPD (2). It's tempting to believe that ACE could be a redox sensor (3,4), activated by hypoxia. This, of course, is a very testable hypothesis, and we encourage labs with the requisite facilities to try. Clinically, our ability to treat sickle cell disease (5) suggests that ACE may indeed be a redox-sensor, as suggested by in silico data (3).

1: Moskowitz DW. Is angiotensin I-converting enzyme a "master" disease gene? Diabetes Technol Ther. 2002;4(5):683-711. PMID: 12458570 (

2: Moskowitz DW. From pharmacogenomics to improved patient outcomes: angiotensin I-converting enzyme as an example. Diabetes Technol Ther. 2002;4(4):519-32.
PMID: 12396747. (

3: Moskowitz DW, Johnson FE. The central role of angiotensin I-converting enzyme in vertebrate pathophysiology. Curr Top Med Chem. 2004;4(13):1433-54. PMID: 15379656 (

4: Moskowitz DW. Acute oxygen-sensing mechanisms. N Engl J Med. 2006 Mar 2;354(9):975-7. PMID: 16510756

5: Williams RM, Moskowitz DW. The prevention of pain from sickle cell disease using trandolapril. J Natl Med Assoc 2007 Mar; 99(3):276-8 (

Competing interests declared: CEO and Chief Medical Officer of GenoMed (, a Next Generation Disease Management company that uses genomics to improve medical outcomes. In addition to halting the progression of COPD, GenoMed has published that effective ACE inhibition can prevent diabetic and hypertensive kidney failure which cause 90% of dialysis world-wide (ref. 2).