Abstract
Stress-induced hypertrophic growth of the myocardium is a pathogenetic milestone in the progression of heart failure. Some evidence suggests that suppression of pathological cardiac hypertrophy per se is a viable target for therapeutic intervention, and cardiomyocyte autophagy is an attractive mechanism for consideration as a means of controlling the hypertrophic response. However, although considerable insights have been gleaned in the molecular mechanisms governing cardiomyocyte autophagy, many details critical to rational targeting of the response remain unknown. Among them, mechanisms underlying the adaptive and maladaptive features of autophagy are obscure. With time and further study, it is possible that this near-ubiquitous cardiac response to stress will emerge as a target for therapeutic manipulation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
