Abstract

Catechins represent a group of polyphenols that possesses various beneficial effects in the cardiovascular system, including protective effects in cardiac ischemia-reperfusion (I/R) injury, a major pathophysiology associated with ischemic heart disease, myocardial infarction, as well as with cardioplegic arrest during heart surgery. In particular, catechin, (−)-epicatechin, and epigallocatechin gallate (EGCG) have been reported to prevent cardiac myocytes from I/R-induced cell damage and I/R-associated molecular changes, finally, resulting in improved cell viability, reduced infarct size, and improved recovery of cardiac function after ischemic insult, which has been widely documented in experimental animal studies and cardiac-derived cell lines. Cardioprotective effects of catechins in I/R injury were mediated via multiple molecular mechanisms, including inhibition of apoptosis; activation of cardioprotective pathways, such as PI3K/Akt (RISK) pathway; and inhibition of stress-associated pathways, including JNK/p38-MAPK; preserving mitochondrial function; and/or modulating autophagy. Moreover, regulatory roles of several microRNAs, including miR-145, miR-384-5p, miR-30a, miR-92a, as well as lncRNA MIAT, were documented in effects of catechins in cardiac I/R. On the other hand, the majority of results come from cell-based experiments and healthy small animals, while studies in large animals and studies including comorbidities or co-medications are rare. Human studies are lacking completely. The dosages of compounds also vary in a broad scale, thus, pharmacological aspects of catechins usage in cardiac I/R are inconclusive so far. Therefore, the aim of this focused review is to summarize the most recent knowledge on the effects of catechins in cardiac I/R injury and bring deep insight into the molecular mechanisms involved and dosage-dependency of these effects, as well as to outline potential gaps for translation of catechin-based treatments into clinical practice.

Highlights

  • IntroductionIn addition to the above-mentioned beneficial effects of catechins on the vasculature, protective effects of various catechin compounds and catechin-rich foods and extracts were reported in I/R injury of the heart, mainly documented in animal studies as well as in in vitro cell-based models of cardiac I/R injury, suggesting promising cardioprotective potential of catechins for the management of patient suffering from ischemic heart disease or myocardial infarction

  • A study performed in cultured neonatal mouse cardiomyocytes (NMCMs) demonstrated that EPI in the 5 μM concentration improved cell viability of NMCMs exposed to 12-h anoxia and reduced apoptosis via activation of the PTEN/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway [69]

  • In vitro models showed strong cardioprotective effects of catechins, mainly epigallocatechin gallate (EGCG), and, catechin and EPI manifested in improved cell viability and reduced apoptosis in cardiac-derived cell lines, such as H9c2 cells, as well as in primary cultures of neonatal rodent cardiomyocytes exposed to H/R injury for various periods of hypoxia/ischemia

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Summary

Introduction

In addition to the above-mentioned beneficial effects of catechins on the vasculature, protective effects of various catechin compounds and catechin-rich foods and extracts were reported in I/R injury of the heart, mainly documented in animal studies as well as in in vitro cell-based models of cardiac I/R injury, suggesting promising cardioprotective potential of catechins for the management of patient suffering from ischemic heart disease or myocardial infarction. Other catechins derived from tea are characterized by different side groups in various positions (substituents or hydroxyl groups placed on the rings or on the galloyl group ((D or B’), Figure 1) All these chemical features determine biological activity of individual catechins, as well as their ability to interact with the surrounding environment [21]. EPI), berries, nuts, and beans [32]

Metabolization of Catechins in the Human Body
Pre-Clinical In Vitro Cell-Based Studies
Pre-Clinical Ex Vivo Studies in Isolated Heart
Pre-Clinical In Vivo Animal Studies
RISK Pathway
Findings
12. Conclusions
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