Molecular biology reportsAug 21, 2026

EGCG's role in controlling cell recycling to treat heart and blood vessel diseases

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Aug 22, 2026

Abstract

Epigallocatechin-3-gallate (EGCG) may restore protective autophagy when it is deficient and suppress excessive autophagic flux when overactivated in cardiovascular diseases.

EGCG is the major catechin in green tea and is associated with protection against cardiovascular diseases (CVDs).
Dysregulation of autophagy may contribute to the progression of CVDs.
EGCG modulates autophagy in a context-dependent manner, varying its effects based on the specific cardiovascular condition.
Multiple signaling pathways, including mTOR and SIRT, may be involved in how EGCG regulates autophagic activity.
Most evidence regarding EGCG's effects on autophagy comes from preclinical studies, with limited direct clinical evidence in humans.
Challenges such as oral bioavailability and clinical translation for EGCG need to be addressed for effective therapeutic application.

Simplified

Green tea is abundant in natural polyphenols and has become one of the most popular healthy non-alcoholic beverages worldwide. Epigallocatechin-3-gallate (EGCG), the major catechin identified in green tea, has been shown to protect against cardiovascular diseases (CVDs). Autophagy degrades damaged or superfluous cellular components. Accumulating in vivo and in vitro studies have indicated that dysregulation of autophagy is implicated in the progression of CVDs. Notably, EGCG exerts a context‑dependent bidirectional modulation of autophagy in CVDs, restoring protective autophagy when it is deficient in conditions such as diabetic cardiomyopathy, and suppressing excessive autophagic flux when it is overactivated in conditions such as myocardial ischemia/reperfusion injury. Emerging studies suggest that EGCG regulates autophagic activity in CVDs through multiple signaling pathways, such as mTOR, SIRT, FoxO, miRNA, and ERK. Notably, most of the available evidence is derived from preclinical studies, and direct clinical evidence supporting EGCG as a therapeutic agent targeting autophagy in humans remains limited. Furthermore, there is an urgent need to address the issues of oral bioavailability and the gap in clinical translation for EGCG. This review comprehensively summarizes the role of EGCG in targeting autophagy and elucidates the associated signaling mechanisms in CVDs, thereby offering systematic insights to guide future research.

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EGCG's role in controlling cell recycling to treat heart and blood vessel diseases

Abstract

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