Cardiac regeneration as an environmental adaptation

Sakaguchi, Akane; Nishiyama, Chihiro; Kimura, Wataru

doi:10.1016/j.bbamcr.2019.118623

Cited by 13 publications

(23 citation statements)

References 163 publications

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“…Among the numerous regulators of cardiomyocyte regeneration, the oxygen environment has received increased attention (Puente et al, 2014;Kimura et al, 2015;Nakada et al, 2017;Sakaguchi et al, 2020). In different species and life stages, oxygen supply and metabolism are distinct.…”

Section: Role Of Oxygen Metabolic Mechanism In Cardiomyocyte Regeneration Oxygen Environment Of Cardiomyocytes Differ Among Species and Lmentioning

confidence: 99%

The Regulatory Role of Oxygen Metabolism in Exercise-Induced Cardiomyocyte Regeneration

Zhou

et al. 2021

Front. Cell Dev. Biol.

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During heart failure, the heart is unable to regenerate lost or damaged cardiomyocytes and is therefore unable to generate adequate cardiac output. Previous research has demonstrated that cardiac regeneration can be promoted by a hypoxia-related oxygen metabolic mechanism. Numerous studies have indicated that exercise plays a regulatory role in the activation of regeneration capacity in both healthy and injured adult cardiomyocytes. However, the role of oxygen metabolism in regulating exercise-induced cardiomyocyte regeneration is unclear. This review focuses on the alteration of the oxygen environment and metabolism in the myocardium induced by exercise, including the effects of mild hypoxia, changes in energy metabolism, enhanced elimination of reactive oxygen species, augmentation of antioxidative capacity, and regulation of the oxygen-related metabolic and molecular pathway in the heart. Deciphering the regulatory role of oxygen metabolism and related factors during and after exercise in cardiomyocyte regeneration will provide biological insight into endogenous cardiac repair mechanisms. Furthermore, this work provides strong evidence for exercise as a cost-effective intervention to improve cardiomyocyte regeneration and restore cardiac function in this patient population.

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Section: Role Of Oxygen Metabolic Mechanism In Cardiomyocyte Regeneration Oxygen Environment Of Cardiomyocytes Differ Among Species and Lmentioning

confidence: 99%

The Regulatory Role of Oxygen Metabolism in Exercise-Induced Cardiomyocyte Regeneration

Zhou

et al. 2021

Front. Cell Dev. Biol.

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“…Patients with SCZ pose unique challenges due to affect, cognition, and socio-demographic factors. Myocardial infarction (MI) and afterward heart failure are the significant causes of death and disability in the developed countries, characterized by acute myocardial ischemia derived from coronary artery occlusion, myocardial injury, and even necrosis ( Lu et al, 2015 ; Sakaguchi et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Schizophrenia Plays a Negative Role in the Pathological Development of Myocardial Infarction at Multiple Biological Levels

et al. 2021

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It has shown that schizophrenia (SCZ) is associated with a higher chance of myocardial infarction (MI) and increased mortality. However, the underlying mechanism is largely unknown. Here, we first constructed a literature-based genetic pathway linking SCZ and MI, and then we tested the expression levels of the genes involved in the pathway by a meta-analysis using nine gene expression datasets of MI. In addition, a literature-based data mining process was conducted to explore the connection between SCZ at different levels: small molecules, complex molecules, and functional classes. The genetic pathway revealed nine genes connecting SCZ and MI. Specifically, SCZ activates two promoters of MI (IL6 and CRP) and deactivates seven inhibitors of MI (ADIPOQ, SOD2, TXN, NGF, ADORA1, NOS1, and CTNNB1), suggesting that no protective role of SCZ in MI was detected. Meta-analysis showed that one promoter of MI (CRP) presented no significant increase, and six out of seven genetic inhibitors of MI demonstrated minor to moderately increased expression. Therefore, the elevation of CRP and inhibition of the six inhibitors of MI by SCZ could be critical pathways to promote MI. Nine other regulators of MI were influenced by SCZ, including two gene families (inflammatory cytokine and IL1 family), five small molecules (lipid peroxide, superoxide, ATP, ascorbic acid, melatonin, arachidonic acid), and two complexes (CaM kinase 2 and IL23). Our results suggested that SCZ promotes the development and progression of MI at different levels, including genes, small molecules, complex molecules, and functional classes.

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“…1 Mammals studied are similar to humans. 2 Mammalian CMs cease their cell-cycle shortly after birth and cardiac injury may accelerate the cessation. 3 , 4 However, CM renewal occurs throughout life, and its rate is very low and decreases with age.…”

Section: Introductionmentioning

confidence: 99%

“…5 , 6 Further studies have shown that the CM renewal 7 and the CM regeneration after injury 8 , 9 were accompanied by few existing CMs reentering the cell cycle. Therefore, the current mainstream understanding of human CM renewal/regeneration is that few CMs retain the proliferative potential, 2 , 7 , 9 and this has led to cardiac regeneration research focusing on CM cell-cycle arrest and reentry. 2 However, the outcome of cell cycle activity is not necessarily CM division but instead can be one of many possibilities.…”

Section: Introductionmentioning

confidence: 99%

Nucleated red blood cells participate in myocardial regeneration in the toad Bufo Gargarizan Gargarizan

Hou

Zhao

et al. 2021

Exp Biol Med (Maywood)

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Heart regeneration is negligible in humans and mammals but remarkable in some ectotherms. Humans and mammals lack nucleated red blood cells (NRBCs), while ectotherms have sufficient NRBCs. This study used Bufo gargarizan gargarizan, a Chinese toad subspecies, as a model animal to verify our hypothesis that NRBCs participate in myocardial regeneration. NRBC infiltration into myocardium was seen in the healthy toad hearts. Heart needle-injury was used as an enlarged model of physiological cardiomyocyte loss. It recovered quickly and scarlessly. NRBC infiltration increased during the recovery. Transwell assay was done to in vitro explore effects of myocardial injury on NRBCs. In the transwell system, NRBCs could infiltrate into cardiac pieces and could transdifferentiate toward cardiomyocytes. Heart apex cautery caused approximately 5% of the ventricle to be injured to varying degrees. In the mildly to moderately injured regions, NRBC infiltration increased and myocardial regeneration started soon after the inflammatory response; the severely damaged region underwent inflammation, scarring, and vascularity before NRBC infiltration and myocardial regeneration, and recovered scarlessly in four months. NRBCs were seen in the newly formed myocardium. Enzyme-linked immunosorbent assay and Western blotting showed that the levels of tumor necrosis factor-α, interleukin- 1β, 6, and11, cardiotrophin-1, vascular endothelial growth factor, erythropoietin, matrix metalloproteinase- 2 and 9 in the serum and/or cardiac tissues fluctuated in different patterns during the cardiac injury-regeneration. Cardiotrophin-1 could induce toad NRBC transdifferentiation toward cardiomyocytes in vitro. Taken together, the results suggest that the NRBC is a cell source for cardiomyocyte renewal/regeneration in the toad; cardiomyocyte loss triggers a series of biological processes, facilitating NRBC infiltration and transition to cardiomyocytes. This finding may guide a new direction for improving human myocardial regeneration.

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Cardiac regeneration as an environmental adaptation

Cited by 13 publications

References 163 publications

The Regulatory Role of Oxygen Metabolism in Exercise-Induced Cardiomyocyte Regeneration

The Regulatory Role of Oxygen Metabolism in Exercise-Induced Cardiomyocyte Regeneration

Schizophrenia Plays a Negative Role in the Pathological Development of Myocardial Infarction at Multiple Biological Levels

Nucleated red blood cells participate in myocardial regeneration in the toad Bufo Gargarizan Gargarizan

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