Mitochondrial dysfunction in heart failure and its therapeutic implications

Liu, Miaosen; Lv, Jialan; Pan, Zhicheng; Wang, Dongfei; Zhao, Liang; Guo, Xiaogang

doi:10.3389/fcvm.2022.945142

Cited by 19 publications

(20 citation statements)

References 139 publications

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“…These results strongly suggest that CSE causes mitochondrial dysfunction, leading to contractile dysfunction and cardiomyocyte death as observed in Figs 1 – 3 . Similar CSE-induced mitochondrial abnormalities have been reported [ 31 ], and emerging evidence has demonstrated that mitochondrial dysfunction contributes to the contractile dysfunction of cardiomyocytes [ 32 ].…”

Section: Discussionsupporting

confidence: 73%

Direct toxicity of cigarette smoke extract on cardiac function mediated by mitochondrial dysfunction in Sprague-Dawley rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes

Matsumura,

Yasuda,

Notomi

et al. 2024

PLoS ONE

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Cigarette smoke has been recognized as a major risk factor for cardiovascular disease. However, its direct effects on rodent and human cardiomyocytes and its cellular mechanisms are not fully understood. In this study, we examined the direct effects of cigarette smoke extract (CSE) on contractile functions, intracellular Ca2+ dynamics, and mitochondrial function using cultured or freshly isolated rat ventricular myocytes and human induced pluripotent stem cell (iPS)-derived cardiomyocytes. In rat cardiomyocytes, CSE (≥0.1%) resulted in a time- and concentration-dependent cessation of spontaneous beating of cultured cardiomyocytes, eventually leading to cell death, which indicates direct toxicity. In addition, 1% CSE reduced contractile function of freshly isolated ventricular myocytes. Similar contractile dysfunction (declined spontaneous beating rate and contractility) was also observed in human iPS-derived cardiomyocytes. Regarding intracellular Ca2+ dynamics, 1% CSE increased the Ca2+ transient amplitude by greatly increasing systolic Ca2+ levels and slightly increasing diastolic Ca2+ levels. CSE also accelerated the decay of Ca2+ transients, and triggered spike-shaped Ca2+ transients in some cells. These results indicate that CSE causes abnormal Ca2+ dynamics in cardiomyocytes. Furthermore, CSE induced a cascade of mitochondrial dysfunctions, including increased mitochondrial reactive oxygen species, opening of mitochondrial permeability transition pore, reduction of mitochondrial membrane potential, and release of cytochrome c from mitochondria. These results suggest that CSE-induced contractile dysfunction and myocardial cell death is caused by abnormal Ca2+ dynamics and subsequent mitochondrial dysregulation, which would result in reduced bioenergetics and activation of cell death pathways.

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Section: Discussionsupporting

confidence: 73%

Direct toxicity of cigarette smoke extract on cardiac function mediated by mitochondrial dysfunction in Sprague-Dawley rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes

Matsumura,

Yasuda,

Notomi

et al. 2024

PLoS ONE

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“…With the development of HF, myocardial fuel gradually shifts from fatty acids to glucose. [42] In addition, mitochondria-mediated cardiomyocyte apoptosis plays a significant role in the development of HF. Impaired mitochondrial structure and function can lead to cell apoptosis, myocardial metabolic remodeling, and chronic HF.…”

Section: Enhancing the Digestion And Absorption Of Lipidsmentioning

confidence: 99%

The role of the gut microbiota and bile acids in heart failure: A review

Shi,

Wei,

Yuan

et al. 2023

Medicine

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Heart failure (HF) is the terminal manifestation of various cardiovascular diseases. Recently, accumulating evidence has demonstrated that gut microbiota are involved in the development of various cardiovascular diseases. Gut microbiota and their metabolites might play a pivotal role in the development of HF. However, previous studies have rarely described the complex role of gut microbiota and their metabolites in HF. In this review, we mainly discussed bile acids (BAs), the metabolites of gut microbiota. We explained the mechanisms by which BAs are involved in the pathogenesis of HF. We also discussed the use of gut microbiota and BAs for treating HF in Chinese medicine, highlighting the advantages of Chinese medicine in treating HF.

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“…The nonspecific high conductance channels of mitochondrial permeability transition pore (mPTP) mediate the transition of mitochondrial permeability. Opening of mPTP leads to collapse of mitochondrial membrane potential, resulting in uncoupling of oxidative phosphorylation and ATP consumption [ 6 , 21 ]. Related studies have shown that changes in mitochondrial permeability are associated with heart failure, hemorrhagic shock, hypertension, cardiomyopathy and cardiac I/R injury [ 14 , 15 , 22 , 23 ].…”

Section: The Role Of Mitochondria In Cardiovascular Systemmentioning

confidence: 99%

“…Cardiomyocytes are one of the cell types with the highest content of mitochondria, and are highly dependent on mitochondrial oxidative phosphorylation to produce ATP. Mitochondria adapt quickly to changing environments to maintain metabolic homeostasis [ 5 , 6 ]. Mitochondria dysfunction involves in the onset and development of CVD.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial transplantation as a novel therapeutic strategy for cardiovascular diseases

Sun

Jiang

et al. 2023

J Transl Med

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Cardiovascular disease (CVD) is the leading cause of noncommunicable disease-related death worldwide, and effective therapeutic strategies against CVD are urgently needed. Mitochondria dysfunction involves in the onset and development of CVD. Nowadays, mitochondrial transplantation, an alternative treatment aimed at increasing mitochondrial number and improving mitochondrial function, has been emerged with great therapeutic potential. Substantial evidence indicates that mitochondrial transplantation improves cardiac function and outcomes in patients with CVD. Therefore, mitochondrial transplantation has profound implications in the prevention and treatment of CVD. Here, we review the mitochondrial abnormalities that occur in CVD and summarize the therapeutic strategies of mitochondrial transplantation for CVD.

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Mitochondrial dysfunction in heart failure and its therapeutic implications

Cited by 19 publications

References 139 publications

Direct toxicity of cigarette smoke extract on cardiac function mediated by mitochondrial dysfunction in Sprague-Dawley rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes

Direct toxicity of cigarette smoke extract on cardiac function mediated by mitochondrial dysfunction in Sprague-Dawley rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes

The role of the gut microbiota and bile acids in heart failure: A review

Mitochondrial transplantation as a novel therapeutic strategy for cardiovascular diseases

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