Hydrogen Sulfide Promotes Cardiomyocyte Proliferation and Heart Regeneration <i>via</i> ROS Scavenging

Pei, Jianqiu; Wang, Fang; Pei, Shengqiang; Bai, Ruifeng; Xu, Cong; Nie, Yu; Chen, Xi

doi:10.1155/2020/1412696

Cited by 21 publications

(14 citation statements)

References 52 publications

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“…H 2 S is endogenously produced in the human body agent and participates in multiple physiologic processes and diseases [ 84 ]. In particular, it exhibits cardioprotective effects in the infarcted hearts [ 85 ]. Miao and colleagues showed that these protective effects were partially mediated by M2 macrophage activation [ 83 ].…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Kim

Nurakhayev

Nurkesh

et al. 2021

IJMS

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Cardiovascular disease is the leading cause of mortality and morbidity around the globe, creating a substantial socio-economic burden as a result. Myocardial infarction is a significant contributor to the detrimental impact of cardiovascular disease. The death of cardiomyocytes following myocardial infarction causes an immune response which leads to further destruction of tissue, and subsequently, results in the formation of non-contractile scar tissue. Macrophages have been recognized as important regulators and participants of inflammation and fibrosis following myocardial infarction. Macrophages are generally classified into two distinct groups, namely, classically activated, or M1 macrophages, and alternatively activated, or M2 macrophages. The phenotypic profile of cardiac macrophages, however, is much more diverse and should not be reduced to these two subsets. In this review, we describe the phenotypes and functions of macrophages which are present in the healthy, as well as the infarcted heart, and analyze them with respect to M1 and M2 polarization states. Furthermore, we discuss therapeutic strategies which utilize macrophage polarization towards an anti-inflammatory or reparative phenotype for the treatment of myocardial infarction.

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Section: Therapeutic Implicationsmentioning

confidence: 99%

Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Kim

Nurakhayev

Nurkesh

et al. 2021

IJMS

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“…These include genes encoding ETC components and ROS eliminator that protect cells from ROS damage and promote cardiomyocyte regeneration (84,103). Pei et al (104) confirmed that hydrogen sulfide (H2S) could scavenge ROS, and hence, cardiomyocytes could re-enter the proliferation cycle. Researchers used propargylglycine (PAG) to inhibit H2S synthesis and found that it promoted the deposition of ROS in the murine neonatal heart and inhibited proliferation of cardiomyocytes (104).…”

Section: Tricarboxylic Acid Cycle Metabolites and Cardiac Regenerationmentioning

confidence: 99%

Metabolic Regulation of Cardiac Regeneration

Duan

Liu²,

Zhan

2022

Front. Cardiovasc. Med.

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The mortality due to heart diseases remains highest in the world every year, with ischemic cardiomyopathy being the prime cause. The irreversible loss of cardiomyocytes following myocardial injury leads to compromised contractility of the remaining myocardium, adverse cardiac remodeling, and ultimately heart failure. The hearts of adult mammals can hardly regenerate after cardiac injury since adult cardiomyocytes exit the cell cycle. Nonetheless, the hearts of early neonatal mammals possess a stronger capacity for regeneration. To improve the prognosis of patients with heart failure and to find the effective therapeutic strategies for it, it is essential to promote endogenous regeneration of adult mammalian cardiomyocytes. Mitochondrial metabolism maintains normal physiological functions of the heart and compensates for heart failure. In recent decades, the focus is on the changes in myocardial energy metabolism, including glucose, fatty acid, and amino acid metabolism, in cardiac physiological and pathological states. In addition to being a source of energy, metabolites are becoming key regulators of gene expression and epigenetic patterns, which may affect heart regeneration. However, the myocardial energy metabolism during heart regeneration is majorly unknown. This review focuses on the role of energy metabolism in cardiac regeneration, intending to shed light on the strategies for manipulating heart regeneration and promoting heart repair after cardiac injury.

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“…Even in basal conditions, aerobic metabolism involves ROS production, thus making O 2 •− and H 2 O 2 physiological intracellular metabolites. In low quantities, ROS act as signalling molecules involved in different pathways, such as cell proliferation, apoptosis and gene expression [ 291 , 292 ]. However, the fact that an important increase in oxidants could target almost all substrates implies the impairment and alteration of all biomolecules, resulting in cell damage and death [ 293 , 294 ].…”

Section: Mechanisms Involved In Fibrosis Progressionmentioning

confidence: 99%

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

Delgado-Valero

Cachofeiro

Martínez‐Martínez

2021

Cells

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Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to the prognosis of patients with cardiac disease. Fibrosis is a common characteristic of organ injury progression that has been proposed not only as a marker but also as an important driver of the pathophysiology of cardiorenal syndromes. Due to the relevance of fibrosis, its study might give insight into the mechanisms and targets that could potentially be modulated to prevent fibrosis development. The aim of this review was to summarize some of the pathophysiological pathways involved in the fibrotic damage seen in cardiorenal syndromes, such as inflammation, oxidative stress and endoplasmic reticulum stress, which are known to be triggers and mediators of fibrosis.

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Hydrogen Sulfide Promotes Cardiomyocyte Proliferation and Heart Regeneration via ROS Scavenging

Cited by 21 publications

References 52 publications

Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Metabolic Regulation of Cardiac Regeneration

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

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