Abstract 407: Role of Apoa1 in Regulating Mitochondrial Function in Acute Myocardial Infarction
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Jg. 32 (2012-05-01)
Online
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Zugriff:
Background: High density lipoprotein (HDL) and apoA-I levels inversely correlate with risk of death from ischemic heart disease; however, the role of apoA-I in myocardial response to ischemia has not been well defined. Methods and results: To test whether apoA-I, the primary HDL apolipoprotein, has an acute anti-inflammatory role in ischemic heart disease, we induced myocardial infarctions in apoA-I -/- and apoA-1 heterozygotic animals. We observed a 52% increase in infarct size as a percent of area at risk in heterozygotic and a 125% increase in apoA-I null animals compared to wild-type mice. Mitochondrial oxidation contributes to tissue damage in ischemic reperfusion injury, and we found a significant defect in the electron transport chain of cardiac myocytes from apoA-I -/- mice. This was localized to the coenzyme Q pool that impaired electron transfer from complex II to complex III. Administration of CoQ10 to apoA-I null animals normalized the cardiac mitochondrial CoQ pool, and it reduced infarct size to that observed of wild type animals. CoQ10 administration did not significantly alter infarct size in wild-type mice. Conclusions: These data identify CoQ pool size and impaired mitochondrial function as major contributors to infarct size in the setting of low HDL/apoA-I. These data suggest a previously unappreciated mechanism for myocardial stunning, cardiac dysfunction, and muscle pain associated with low HDL/apoA-I levels that can be corrected by CoQ10 supplementation and suggest populations of patients that may particularly benefit from CoQ10 supplementation.
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Abstract 407: Role of Apoa1 in Regulating Mitochondrial Function in Acute Myocardial Infarction
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Autor/in / Beteiligte Person: | Marc S Penn ; Latchoumycandane, Calivarathan ; Thomas M McIntyre ; Edward J Lesnefsky |
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Zeitschrift: | Arteriosclerosis, Thrombosis, and Vascular Biology, Jg. 32 (2012-05-01) |
Veröffentlichung: | Ovid Technologies (Wolters Kluwer Health), 2012 |
Medientyp: | unknown |
ISSN: | 1524-4636 (print) ; 1079-5642 (print) |
DOI: | 10.1161/atvb.32.suppl_1.a407 |
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