Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy

Wang, Shawn Yongshun; Zhu, Siyu; Wu, Jiarui; Zhang, Maomao; Xu, Yousheng; Xu, Wei; Cui, Jinjin; Yu, Bo; Cao, Wei; Liu, Jingjin

doi:10.1007/s00109-019-01861-2

Cited by 51 publications

(45 citation statements)

References 41 publications

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“…These lipid metabolism toxicants can interfere with normal cellular signals; result in myocardial cell apoptosis, cell damage, and mitochondrial dysfunction; and ultimately lead to reduced cardiac contractile function [ 73 , 74 ]. Therefore, abnormal cardiac fat metabolism is an important cause of DCM [ 75 , 76 ].…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology-Based Strategy Reveals the Effects of Hedysarum multijugum Maxim.-Radix Salviae Compound on Oxidative Capacity and Cardiomyocyte Apoptosis in Rats with Diabetic Cardiomyopathy

Zhang

Yuan

et al. 2020

BioMed Research International

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Objective. To explore the effects of the Hedysarum multijugum Maxim.-Radix Salviae compound (Huangqi-Danshen Compound (HDC)) on oxidative capacity and cardiomyocyte apoptosis in rats with diabetic cardiomyopathy by a network pharmacology-based strategy. Methods. Traditional Chinese Medicine (TCM)@Taiwan, TCM Systems Pharmacology Database and Analysis Platform (TCMSP), TCM Integrated Database (TCMID), and High-Performance Liquid Chromatography (HPLC) technology were used to obtain and screen HDC’s active components, and the PharmMapper database was used to predict HDC human target protein targets. The DCM genes were collected from the GeneCards and OMIM databases, and the network was constructed and analyzed by Cytoscape 3.7.1 and the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Finally, HDC was used to intervene in diabetic cardiomyopathy (DCM) model rats, and important biological processes and signaling pathways were verified using techniques such as immunohistochemistry. Results. A total of 176 of HDC’s active components and 442 potential targets were obtained. The results of network analysis show that HDC can regulate DCM-related biological processes (such as negative regulation of the apoptotic process, response to hypoxia, the steroid hormone-mediated signaling pathway, cellular iron ion homeostasis, and positive regulation of phosphatidylinositol 3-kinase signaling) and signaling pathways (such as the HIF-1 signaling pathway, the estrogen signaling pathway, insulin resistance, the PPAR signaling pathway, the VEGF signaling pathway, and the PI3K-Akt signaling pathway). Animal experiments show that HDC can reduce fasting plasma glucose (FPG), HbA1c, and malondialdehyde (MDA) and increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) ( P < 0.05 ). The results of immunohistochemistry showed that HDC can regulate the protein expression of apoptosis-related signaling pathways in DCM rats ( P < 0.05 ). Conclusion. It was initially revealed that HDC improves DCM through its antiapoptotic and anti-inflammatory effects. HDC may play a therapeutic role by improving cardiomyocyte apoptosis in DCM rats.

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Section: Discussionmentioning

confidence: 99%

Network Pharmacology-Based Strategy Reveals the Effects of Hedysarum multijugum Maxim.-Radix Salviae Compound on Oxidative Capacity and Cardiomyocyte Apoptosis in Rats with Diabetic Cardiomyopathy

Zhang

Yuan

et al. 2020

BioMed Research International

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“…Further, decreases in oxidative stress and ROS production have also been detected in mice with diabetic cardiomyopathy following 16 weeks of running exercise (Wang et al, 2020). Moreover, 8 weeks of resistance exercise (Effting et al, 2019) or swim training (de Farias et al, 2013) can modulate redox imbalance and reduce oxidative damage in the myocardium in mice with diet-induced obesity.…”

Section: Exercise Modulates Oxidative Stress In Cardiomyocytesmentioning

confidence: 97%

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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“…Exercise protects the heart against ROS accumulation during the development of DCM. In a diabetic mouse model, exercise ameliorates blood pressure and systolic dysfunction and improves mitochondrial function by shifting energy metabolism from fatty acid to glucose oxidation (Wang et al, 2020). Accordingly, in a rat model of diabetes, resistance exercise reduces reactive oxygen species production and improves mitochondrial function.…”

Section: Diabetic Cardiomyopathymentioning

confidence: 99%

Physical Exercise: A Novel Tool to Protect Mitochondrial Health

2021

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Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.

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Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy

Cited by 51 publications

References 41 publications

Network Pharmacology-Based Strategy Reveals the Effects of Hedysarum multijugum Maxim.-Radix Salviae Compound on Oxidative Capacity and Cardiomyocyte Apoptosis in Rats with Diabetic Cardiomyopathy

Network Pharmacology-Based Strategy Reveals the Effects of Hedysarum multijugum Maxim.-Radix Salviae Compound on Oxidative Capacity and Cardiomyocyte Apoptosis in Rats with Diabetic Cardiomyopathy

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

Physical Exercise: A Novel Tool to Protect Mitochondrial Health

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