Melatonin fine-tunes intracellular calcium signals and eliminates myocardial damage through the IP3R/MCU pathways in cardiorenal syndrome type 3

Wang, Jin; Toan, Sam; Li, Ruibin; Zhou, Hao

doi:10.1016/j.bcp.2020.113832

Cited by 57 publications

(49 citation statements)

References 57 publications

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“…Mitochondrial membrane potential was observed using a mitochondrial membrane potential assay kit with JC-1 (Beyotime, China, Cat. No:C2006) as previously described ( Wang et al, 2020a ).…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

Zheng¹,

Lu²

2020

Front. Cell Dev. Biol.

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Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction is an initial step toward atherosclerosis development. Mitochondria damage correlates with ox-LDL-induced endothelial injury through an undefined mechanism. We explored the role of optic atrophy 1 (Opa1)-related mitochondrial fusion and mitophagy in ox-LDL-treated endothelial cells, focusing on mitochondrial damage and cell apoptosis. Oxidized low-density lipoprotein treatment reduced endothelial cell viability by increasing apoptosis. Endothelial cell proliferation and migration were also impaired by ox-LDL. At the molecular level, mitochondrial dysfunction was induced by ox-LDL, as demonstrated by decreased mitochondrial membrane potential, increased mitochondrial reactive oxygen species production, augmented mitochondrial permeability transition pore openings, and elevated caspase-3/9 activity. Mitophagy and mitochondrial fusion were also impaired by ox-LDL. Opa1 overexpression reversed this effect by increasing endothelial cell viability and decreasing apoptosis. Interestingly, inhibition of mitophagy or mitochondrial fusion through transfection of siRNAs against Atg5 or Mfn2, respectively, abolished the protective effects of Opa1. Our results illustrate the role of Opa1-related mitochondrial fusion and mitophagy in sustaining endothelial cell viability and mitochondrial homeostasis under ox-LDL stress.

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“…Mitochondrial membrane potential was observed using a mitochondrial membrane potential assay kit with JC-1 (Beyotime, China, Cat. No:C2006) as previously described ( Wang et al, 2020a ).…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

Zheng¹,

Lu²

2020

Front. Cell Dev. Biol.

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“…Cardiomyocytes in the control group were cultured in 5.5 mmol/L standard glucose medium (control group), while those in the in vitro hyperglycemia injury model group were cultured in 25 mmol/L high-glucose DMEM for 12 h. Both types of medium were supplemented with 10% fetal bovine serum (Gibco, C11995500), 100 IU/ml penicillin and 100 μg/ml streptomycin. The cells were incubated in 95% air and 5% CO 2 (Wang et al, 2020a).…”

Section: Cardiomyocyte Culture and Treatmentmentioning

confidence: 99%

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

et al. 2021

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Matrine, an active component of Sophora flavescens Ait root extracts, has been used in China for years to treat cancer and viral hepatitis. In the present study, we explored the effects of matrine on hyperglycemia-treated cardiomyocytes. Cardiomyocyte function, oxidative stress, cellular viability, and mitochondrial fusion were assessed through immunofluorescence, quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assays, and RNA interference. Matrine treatment suppressed hyperglycemia-induced oxidative stress in cardiomyocytes by upregulating transcription of nuclear factor erythroid 2-like 2 and heme oxygenase-1. Matrine also improved cardiomyocyte contractile and relaxation function during hyperglycemia, and it reduced hyperglycemia-induced cardiomyocyte death by inhibiting mitochondrial apoptosis. Matrine treatment increased the transcription of mitochondrial fusion-related genes and thus attenuated the proportion of fragmented mitochondria in cardiomyocytes. Inhibiting mitochondrial fusion by knocking down mitofusin 2 (Mfn2) abolished the cardioprotective effects of matrine during hyperglycemia. These results demonstrate that matrine could be an effective drug to alleviate hyperglycemia-induced cardiomyocyte damage by activating Mfn2-induced mitochondrial fusion.

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“…Normal mouse cardiomyocytes were isolated from 1-day-old C57BL/6 mice (Wang et al, 2020a). Heart ventricles were cut and minced into 1 mm 3 pieces and digested with 0.2% collagenase II for 2 h on ice.…”

Section: Primary Cardiomyocyte Culturementioning

confidence: 99%

RETRACTED: Opa1 Reduces Hypoxia-Induced Cardiomyocyte Death by Improving Mitochondrial Quality Control

Xin

et al. 2020

Front. Cell Dev. Biol.

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Mitochondrial dysfunction contributes to cardiovascular disorders, especially postinfarction cardiac injury, through incompletely characterized mechanisms. Among the latter, increasing evidence points to alterations in mitochondrial quality control, a range of adaptive responses regulating mitochondrial morphology and function. Optic atrophy 1 (Opa1) is a mitochondrial inner membrane GTPase known to promote mitochondrial fusion. In this study, hypoxia-mediated cardiomyocyte damage was induced to mimic post-infarction cardiac injury in vitro. Loss-and gain-of-function assays were then performed to evaluate the impact of Opa1 expression on mitochondrial quality control and cardiomyocyte survival and function. Hypoxic stress reduced cardiomyocyte viability, impaired contractile/relaxation functions, and augmented the synthesis of proinflammatory mediators. These effects were exacerbated by Opa1 knockdown, and significantly attenuated by Opa1 overexpression. Mitochondrial quality control was disturbed by hypoxia, as reflected by multiple mitochondrial deficits; i.e., increased fission, defective fusion, impaired mitophagy, decreased biogenesis, increased oxidative stress, and blunted respiration. By contrast, overexpression of Opa1 normalized mitochondrial quality control and sustained cardiomyocyte function. We also found that ERK, AMPK, and YAP signaling can regulate Opa1 expression. These results identify Opa1 as a novel regulator of mitochondrial quality control and highlight a key role for Opa1 in protecting cardiomyocytes against post-infarction cardiac injury.

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Melatonin fine-tunes intracellular calcium signals and eliminates myocardial damage through the IP3R/MCU pathways in cardiorenal syndrome type 3

Cited by 57 publications

References 57 publications

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

RETRACTED: Opa1 Reduces Hypoxia-Induced Cardiomyocyte Death by Improving Mitochondrial Quality Control

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