Therapeutic potentials of modulating autophagy in pathological cardiac hypertrophy.

Abstract

Cardiac hypertrophy is an adaptive response to increased overload, which is induced by various physiological or pathological stimuli. It is a common pathological process of a variety of cardiovascular diseases, which eventually leads to heart failure. Several lines of evidence suggested that autophagy as a double-edged sword was involved in cardiac hypertrophy. Autophagy, with a typical feature of double-membrane vesicle called the autophagosome, is a highly conserved lysosomal degradation process and plays an important role in the regulation of diverse physiologic and pathologic processes. However, the exact mechanism underlying the role of autophagy in regulating cardiac hypertrophy remains largely unknown. Here, we comprehensively characterize the dual effects of autophagy in promoting or inhibiting cardiac hypertrophy under different conditions. Moreover, we summarize the potential therapeutic effects of autophagy modulators on pathological cardiac hypertrophy. Finally, we discuss the advantages and challenges of autophagic modulators for the therapy of pathological cardiac hypertrophy.

The molecular mechanism of MiR-26a-5p regulates excessive autophagy and activates NLRP3 inflammasome to mediate cardiomyocyte hypertrophy

“…Although some genes and signalling pathways were involved in the pathological process of cardiac hypertrophy, their mechanism has yet to be fully elucidated, and further research is needed [7][8][9][10] .…”