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Review
. 2022 Mar 15;14(3):1952-1968.
eCollection 2022.

Research on natural products from traditional Chinese medicine in the treatment of myocardial ischemia-reperfusion injury

Wenyu Bu  1 , Zhaoyang Zhang  2 , Dickson Kofi Wiredu Ocansey  3   4 , Zhihua Yu  5 , Xiao Yang  1 , Zhitong Liu  1 , Xinyu Wang  1 , Yuhe Ke  1   5
Affiliations
Review

Research on natural products from traditional Chinese medicine in the treatment of myocardial ischemia-reperfusion injury

Wenyu Bu et al. Am J Transl Res. .

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is a complicated pathologic process that involves multiple factors including oxidative stress (free radical damage), inflammatory response, calcium overloading, and apoptosis in cardiomyocytes. According to Traditional Chinese Medicine (TCM), MIRI belongs to the categories of "chest numbness", "palpitations" and "angina pectoris". Present data indicate that the application of TCM in myocardial ischemia-reperfusion injury is promising and continues to attract research attention. While the efficacy of Chinese herbal medicine has been well-proven, the underlying molecular mechanisms remain elusive. The common proven mechanisms of Chinese herbal medicine in the treatment of MIRI include regulating lipid metabolism, protecting mitochondria, and improving energy metabolism, attenuating calcium (Ca2+) overload, scavenging oxygen free radicals, inhibiting apoptosis, and reducing autophagy. Others are the regulation of inflammatory cytokine expressions and healing of inflammatory lesions, modulation of cell signaling pathways, improvement of endothelial cell function, and protection of myocardial cells. In this review, we highlight recent studies that focus on elucidating these molecular mechanisms and the therapeutic effects of natural compounds deriving from TCM in MIRI, to ascertain the research progress made and the prospects in this field.

Keywords: Myocardial ischemia-reperfusion injury; compound Chinese medicine; ingredients of traditional Chinese medicine; traditional Chinese medicine therapy.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Main regulatory mechanisms of apoptosis and necroptosis in MIRI. The exogenous and endogenous pathways of apoptosis are regulated by death receptors as shown in (A). The link of RIP1 to apoptosis and necroptosis is illustrated in (B). PI3K: phosphoinositide-3-kinase; Akt: protein kinase B; NF-κB: nuclear factor kappa B; JAK2: Janus Kinase 2; STAT3: signal transducer and activator of transcription 3; ATF6: activating transcription factor 6; MAPK: mitogen-activated protein kinase; PERK: (PKR)-like ER kinase; Bcl-2: B-lymphocytoma-2 gene; Bax: Bcl2 associated X protein; MPTP: mitochondrial permeability transition pore; ERS: ER Stress; RIP1: receptor-interacting protein kinase 1; RIP3: receptor-interacting protein kinase 3; MLKL: mixed lineage kinase domain-like protein.
Figure 2
Figure 2
The main regulatory mechanisms of autophagy and pyroptosis in MIRI. The chain of molecular reactions associated with autophagy and apoptosis in MIRI is presented in (A). The inflammasome-associated inflammatory caspases activation of pyroptosis is illustrated in (B). AMPK: AMP-activated protein kinase; mTOR: mammalian target of Rapamycin; ULK1: unc-51-like kinase 1; BNIP3: BCL2 interacting protein 3; PINK1: PTEN-induced kinase 1; Parkin: Parkinson juvenile disease protein 2; LC3: microtubule-associated protein light chain 3; TLR: toll-like receptor; MyD88: myeloid differentiation factor 88; IκBα: recombinant inhibitory subunit of NF-κB alpha; NLRP3: NOD-like receptor protein 3; ASC: apoptosis-associated speck-like protein containing CARD; IL-1β: interleukin-1β; GSDMD: pro-pyroptotic factor gasdermin D; GSDMD-NT: GSDMD N-terminal.
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