MARK4 controls ischaemic heart failure through microtubule detyrosination.

ABSTRACT: Myocardial infarction is a major cause of premature death in adults. Compromised cardiac function after myocardial infarction leads to chronic heart failure with systemic health complications and a high mortality rate¹. Effective therapeutic strategies are needed to improve the recovery of cardiac function after myocardial infarction. More specifically, there is a major unmet need for a new class of drugs that can improve cardiomyocyte contractility, because inotropic therapies that are currently available have been associated with high morbidity and mortality in patients with systolic heart failure^2,3 or have shown a very modest reduction of risk of heart failure⁴. Microtubule detyrosination is emerging as an important mechanism for the regulation of cardi

SUBMITTER: Yu X 

PROVIDER: S-EPMC7612144 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature