MCED: A newly-discovered mechanism of endothelial cell death
Using a patented laboratory test, we have discovered a new cell death pathway in endothelial cells which we refer to as Massively Calcified Endosomal Death (MCED). Exploitation of this pathway may afford an effective approach to the treatment of cancer and to the prevention and treatment of atherosclerotic vascular disease, heart attack, and stroke.
MCED in Coronary and Vascular Disease
“Cholesterol levels might not matter. The most important cause of heart attack, stroke, and arterial blockage might be the presence or absence of circulating MCED factors.”
The underlying mechanisms of atherosclerotic vascular disease are not well-understood by scientists. It is not known, for example, precisely how pathogenic lipids trigger an inflammatory response in arterial walls. Neither is it well-established how atherosclerotic arteries become calcified. Likewise, the mechanisms underlying the cause of calcific cardiac valvular disease (e.g. mitral and aortic stenosis) remain largely unknown. And why are cholesterol and other lipid levels only imperfect predictors of coronary artery disease?
We have discovered a previously unknown biological mechanism that explains much of what is not understood about arterial blockage and heart disease. Understanding the mechanism will allow for development of drugs that control it.
We postulate that massively calcified endosomal death is the triggering event for both vascular inflammation and vascular calcium accumulation. Interruption of the MCED pathway, using MCED-targeted drugs, may offer the most potent and specific approach to the prevention and treatment of coronary vascular disease.
MCED in Cancer
The highly-promising treatment paradigm of anti-angiogenic therapy has so far achieved only moderate success. Anti-angiogenic research is severely hindered by the inadequacy of disease models and predictive biomarkers. Acquired resistance to anti-angiogenic agents is poorly understood, as is the mechanism through which treatment with bevacizumab (Avastin) increases the risk of cardiovascular disease
MCED induction - precisely the opposite of the goal in heart disease - may be effective in treating cancer.
“Activation of the MCED pathway may enhance effectiveness of anticancer drugs that work by destroying blood vessels necessary to feed the growth of the cancer.”
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