Aerobic exercise alleviates oxidative stress-induced apoptosis in kidneys of myocardial infarction mice by inhibiting ALCAT1 and activating FNDC5/Irisin signaling pathway

Wu, Fangnan; Li, Zhuo; Cai, Mengxin; Xi, Yue; Xu, Zujie; Zhang, Zezhou; Li, Hangzhuo; Zhu, Wenyao; Tian, Zhenjun

doi:10.1016/j.freeradbiomed.2020.06.038

Cited by 60 publications

(38 citation statements)

References 42 publications

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“…It has been reported that both swimming and treadmill protocol enhanced the Irisin expression in MI rat’s serum [ 50 , 51 ]. Similarly, previous studies in our laboratory confirmed that aerobic exercise can significantly increase the Irisin expression in the kidney of MI mice and simultaneously inhibit the oxidative stress [ 48 ]. Our current results showed that for MI mice, the resistance exercise significantly enhanced the expression of Irisin, increased the activity of T-SOD and SOD2 expression, decreased the content of serum MDA, and improved the level of oxidative stress in myocardium.…”

Section: Discussionsupporting

confidence: 75%

“…The previous studies demonstrated that MI led to SOD inactivity, increased MDA and reactive oxygen species (ROS) accumulation, and broke the balance of oxidation and antioxidant [ 43 , 44 , 45 ]. Exercise intervention can significantly up-regulate the expression of Irisin and SOD activity in the heart, liver, kidney and other organs of mice under the circumstances of ischemia and hypoxia, while reduce the level of MDA and ROS [ 46 , 47 , 48 ]. Irisin contributed to the maintaining oxidative balance in organs and tissues [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

“…AICAR proved to play a cardioprotective role as an AMPK agonist in a variety of disease models (e.g., hypertensive [ 65 ], acute kidney injury [ 66 ], cardiac hypoxia [ 67 ]). The previous research also used AICAR as AMPK agonist to explore the protective effect of exercise on ischemic myocardium [ 44 , 48 ]. This study showed that AICAR could significantly up-regulate the expression of AMPK in H9C2 cells, activate the PINK1/Parkin-LC3/P62 signaling pathway, and enhance mitophagy.…”

Section: Discussionmentioning

confidence: 99%

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Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

Qin

Liang

et al. 2021

Biomedicines

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Myocardial infarction is the major cause of death in cardiovascular disease. In vitro and in vivo models are used to find the exercise mode which has the most significant effect on myocardial irisin/FNDC5 expression and illuminate the cardioprotective role and mechanisms of exercise-activated myocardial irisin/FNDC5-PINK1/Parkin-mediated mitophagy in myocardial infarction. The results indicated that expression of irisin/FNDC5 in myocardium could be up-regulated by different types of exercise and skeletal muscle electrical stimulation, which then promotes mitophagy and improves cardiac function and the effect of resistance exercise. Resistance exercise can improve cardiac function by activating the irisin/FNDC5-PINK1/Parkin-LC3/P62 pathway, regulating mitophagy and inhibiting oxidative stress. OPA1 may play an important role in the improvement of cardiac function and mitophagy pathway in myocardial infarction mice by irisin-mediated resistance exercise. Resistance exercise is expected to become an effective therapeutic way to promote myocardial infarction rehabilitation.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

Qin

Liang

et al. 2021

Biomedicines

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“…The AMPK–SIRT1 signaling pathway is vital for improving mitochondrial energy metabolism ( Tian et al, 2019 ). The AMPK/SIRT1/PGC-1α pathway, by participating in the alleviation of the levels of oxidative stress and apoptosis following MI ( Wu et al, 2020 ), can protect the mitochondrial biogenesis and functions in cerebral ischemic stroke ( Gao et al, 2020 ). In the H 2 O 2 model, TMZ activated the SIRT1–AMPK pathway.…”

Section: Discussionmentioning

confidence: 99%

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

et al. 2021

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Myocardial energy metabolism (MEM) is an important factor of myocardial injury. Trimetazidine (TMZ) provides protection against myocardial ischemia/reperfusion injury. The current study set out to evaluate the effect and mechanism of TMZ on MEM disorder induced by myocardial infarction (MI). Firstly, a MI mouse model was established by coronary artery ligation, which was then treated with different concentrations of TMZ (5, 10, and 20 mg kg–1 day–1). The results suggested that TMZ reduced the heart/weight ratio in a concentration-dependent manner. TMZ also reduced the levels of Bax and cleaved caspase-3 and promoted Bcl-2 expression. In addition, TMZ augmented adenosine triphosphate (ATP) production and superoxide dismutase (SOD) activity induced by MI and decreased the levels of lipid peroxide (LPO), free fatty acids (FFA), and nitric oxide (NO) in a concentration-dependent manner (all P < 0.05). Furthermore, an H2O2-induced cell injury model was established and treated with different concentrations of TMZ (1, 5, and 10 μM). The results showed that SIRT1 overexpression promoted ATP production and reactive oxygen species (ROS) activity and reduced the levels of LPO, FFA, and NO in H9C2 cardiomyocytes treated with H2O2 and TMZ. Silencing SIRT1 suppressed ATP production and ROS activity and increased the levels of LPO, FFA, and NO (all P < 0.05). TMZ activated the SIRT1–AMPK pathway by increasing SIRT1 expression and AMPK phosphorylation. In conclusion, TMZ inhibited MI-induced myocardial apoptosis and MEM disorder by activating the SIRT1–AMPK pathway.

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“…Aerobic exercise also promotes FNDC5/irisin and PGC-1α signaling, slowing down the development of kidney and cardiac injury. Irisin recombinant protein attenuates hydrogen peroxide (H 2 O 2) -induced oxidative stress and cell dysfunction [ 105 ].…”

Section: Treatment Options For Osteoporosis Via Mitochondrial Energetics and Rosmentioning

confidence: 99%

Biophysical Modulation of the Mitochondrial Metabolism and Redox in Bone Homeostasis and Osteoporosis: How Biophysics Converts into Bioenergetics

Wang

Chen

et al. 2021

Antioxidants

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Bone-forming cells build mineralized microstructure and couple with bone-resorbing cells, harmonizing bone mineral acquisition, and remodeling to maintain bone mass homeostasis. Mitochondrial glycolysis and oxidative phosphorylation pathways together with ROS generation meet the energy requirement for bone-forming cell growth and differentiation, respectively. Moderate mechanical stimulations, such as weight loading, physical activity, ultrasound, vibration, and electromagnetic field stimulation, etc., are advantageous to bone-forming cell activity, promoting bone anabolism to compromise osteoporosis development. A plethora of molecules, including ion channels, integrins, focal adhesion kinases, and myokines, are mechanosensitive and transduce mechanical stimuli into intercellular signaling, regulating growth, mineralized extracellular matrix biosynthesis, and resorption. Mechanical stimulation changes mitochondrial respiration, biogenesis, dynamics, calcium influx, and redox, whereas mechanical disuse induces mitochondrial dysfunction and oxidative stress, which aggravates bone-forming cell apoptosis, senescence, and dysfunction. The control of the mitochondrial biogenesis activator PGC-1α by NAD+-dependent deacetylase sirtuins or myokine FNDC/irisin or repression of oxidative stress by mitochondrial antioxidant Nrf2 modulates the biophysical stimulation for the promotion of bone integrity. This review sheds light onto the roles of mechanosensitive signaling, mitochondrial dynamics, and antioxidants in mediating the anabolic effects of biophysical stimulation to bone tissue and highlights the remedial potential of mitochondrial biogenesis regulators for osteoporosis.

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Aerobic exercise alleviates oxidative stress-induced apoptosis in kidneys of myocardial infarction mice by inhibiting ALCAT1 and activating FNDC5/Irisin signaling pathway

Cited by 60 publications

References 42 publications

Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

Biophysical Modulation of the Mitochondrial Metabolism and Redox in Bone Homeostasis and Osteoporosis: How Biophysics Converts into Bioenergetics

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