Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction

In conclusion, our data provide the evidence that impaired cardiac BCAA catabolism directly contributes to post-MI cardiac dysfunction and remodeling. Moreover, improving cardiac BCAA catabolic defects may be a promising therapeutic strategy against post-MI HF.
Source: AJP: Heart and Circulatory Physiology - Category: Cardiology Authors: Tags: Integrative Cardiovascular Physiology and Pathophysiology Source Type: research