Review article
Molecular machinery and interplay of apoptosis and autophagy in coronary heart disease

https://doi.org/10.1016/j.yjmcc.2019.09.001Get rights and content
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open access

Highlights

  • Apoptosis and autophagy have complex interplays via different pathways.

  • Apoptosis promotes the pathogenesis of CHD generally.

  • Autophagy resists against myocardial ischemia and postischemia cardiac remodeling.

  • Autophagy plays controversial roles in I/R injury and coronary atherosclerosis.

  • Regulation of apoptosis and autophagy is an appealing therapy for CHD.

Abstract

Coronary heart disease (CHD) is a common heart disease and the leading cause of cardiovascular death. Apoptosis and autophagy are two forms of programmed cell deaths which participate in the pathogenesis, development and prognosis of CHD. They are activated by several different pathways respectively and can interact with each other through the Beclin 1-Bcl-2/Bcl-xL complex, mTOR, TRAIL, TNF-α, ER stress and nucleus p53 pathways. Excessive apoptosis can promote myocardial ischemia, ischemia/reperfusion (I/R) injury, post-ischemia cardiac remodeling and coronary atherosclerosis except for VSMC-induced atherosclerosis progress. In contrast, activated autophagy protects heart from myocardial ischemia injury and post-ischemia cardiac remodeling, but can exert controversial effects on I/R injury and coronary atherosclerosis. Therefore, considering the pathological significance and mechanisms of apoptosis and autophagy underlying CHD, therapeutic implication of targeting apoptosis and autophagy is obvious. Fortunately, some therapeutic drugs and pharmacologic compounds involving mTOR inhibitor and AMPK activator have been reported to regulate apoptosis and autophagy. Although recent studies are limited and insufficient, they have pointed out the complex interplay between apoptosis and autophagy and further provided treatment concept for CHD by balancing the switch between the two responses.

Keywords

Coronary heart disease
Apoptosis
Autophagy
Molecular machinery
Interplay
Therapeutic implication

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These authors contributed equally to this work