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Title:
CAV3 alleviates diabetic cardiomyopathy via inhibiting NDUFA10-mediated mitochondrial dysfunction | Journal of Translational Medicine
Description:
Background The progression of diabetic cardiomyopathy (DCM) is noticeably influenced by mitochondrial dysfunction. Variants of caveolin 3 (CAV3) play important roles in cardiovascular diseases. However, the potential roles of CAV3 in mitochondrial function in DCM and the related mechanisms have not yet been elucidated. Methods Cardiomyocytes were cultured under high-glucose and high-fat (HGHF) conditions in vitro, and db/db mice were employed as a diabetes model in vivo. To investigate the role of CAV3 in DCM and to elucidate the molecular mechanisms underlying its involvement in mitochondrial function, we conducted Liquid chromatography tandem mass spectrometry (LCâMS/MS) analysis and functional experiments. Results Our findings demonstrated significant downregulation of CAV3 in the cardiac tissue of db/db mice, which was found to be associated with cardiomyocyte apoptosis in DCM. Importantly, cardiac-specific overexpression of CAV3 effectively inhibited the progression of DCM, as it protected against cardiac dysfunction and cardiac remodeling associated by alleviating cardiomyocyte mitochondrial dysfunction. Furthermore, mass spectrometry analysis and immunoprecipitation assays indicated that CAV3 interacted with NDUFA10, a subunit of mitochondrial complex I. CAV3 overexpression reduced the degradation of lysosomal pathway in NDUFA10, restored the activity of mitochondrial complex I and improved mitochondrial function. Finally, our study demonstrated that CAV3 overexpression restored mitochondrial function and subsequently alleviated DCM partially through NDUFA10. Conclusions The current study provides evidence that CAV3 expression is significantly downregulated in DCM. Upregulation of CAV3 interacts with NDUFA10, inhibits the degradation of lysosomal pathway in NDUFA10, a subunit of mitochondrial complex I, restores the activity of mitochondrial complex I, ameliorates mitochondrial dysfunction, and thereby protects against DCM. These findings indicate that targeting CAV3 may be a promising approach for the treatment of DCM.
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Keywords {đ}
cav, mice, mitochondrial, pubmed, ndufa, article, dbdb, overexpression, google, scholar, cardiomyocytes, fig, dysfunction, cas, diabetic, dcm, analysis, cardiac, levels, staining, function, diabetes, cardiomyopathy, complex, protein, china, cells, data, expression, hghf, mitochondria, hearts, figure, central, study, heart, glucose, additional, downregulation, cell, quantitative, file, treated, apoptosis, ros, aavcav, partially, western, blotting, images,
Topics {âď¸}
terminal deoxynucleotidyl transferase-mediated nick end labeling db/dbâ+âaav-ctrlâ+âaav-shnc group db/dbâ+âaav-cav3â+âaav-shnc group db/dbâ+âaav-ctrlâ+âaav-shndufa10 group db/dbâ+âaav-cav3â+âaav-shndufa10 group hrp-conjugated goat anti-mouse aav9-cav3-shndufa10-treated db/db mice impairing adipor1/caveolin-3/stat3 signaling impairing caveolin-3-modulated pi3k/akt high-glucose-high-fatty-acid myocardial ischemia/reperfusion injury ndufs1-mediated mitochondrial dysfunction representative transmission electron microscope images lcâms/ms analysis lcâms/ms analysis hrp-conjugated anti-rabbit article download pdf db/dbâ+âaav9-cav3 groups insulin-resistance-induced heart disease dependent antioxidant response annexin v-fitc db/dbâ+âaav9-ctrl quantitative real-time- pcr beta-actin rna expression lcâms/ms mitochondrial dysfunction-related genes anti-dna/rna damage restoring caveolin-3/enos signaling specifically leptin receptor-deficient restoring caveolin-3/akt signaling db/db mouse hearts spec-ally life technology endoplasmic reticulum stress male db/db mice db/db mice transfected anti-cav3 antibody pulled db/db mice hearts db/db mice treated promotes cell-cycle progression aav9-cav3 treatment compared reactive oxygen species db/db mice groups aav9-ctrl-shnc anti-rabbit secondary antibodies cardiac diastolic function ameliorates mitochondrial dysfunction mass spectrometry analysis db/db mice observed wheat germ agglutinin transmission electron microscopy
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- How does pioglitazone prevent progression of impaired glucose tolerance to diabetes?
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headline:CAV3 alleviates diabetic cardiomyopathy via inhibiting NDUFA10-mediated mitochondrial dysfunction
description:The progression of diabetic cardiomyopathy (DCM) is noticeably influenced by mitochondrial dysfunction. Variants of caveolin 3 (CAV3) play important roles in cardiovascular diseases. However, the potential roles of CAV3 in mitochondrial function in DCM and the related mechanisms have not yet been elucidated. Cardiomyocytes were cultured under high-glucose and high-fat (HGHF) conditions in vitro, and db/db mice were employed as a diabetes model in vivo. To investigate the role of CAV3 in DCM and to elucidate the molecular mechanisms underlying its involvement in mitochondrial function, we conducted Liquid chromatography tandem mass spectrometry (LCâMS/MS) analysis and functional experiments. Our findings demonstrated significant downregulation of CAV3 in the cardiac tissue of db/db mice, which was found to be associated with cardiomyocyte apoptosis in DCM. Importantly, cardiac-specific overexpression of CAV3 effectively inhibited the progression of DCM, as it protected against cardiac dysfunction and cardiac remodeling associated by alleviating cardiomyocyte mitochondrial dysfunction. Furthermore, mass spectrometry analysis and immunoprecipitation assays indicated that CAV3 interacted with NDUFA10, a subunit of mitochondrial complex I. CAV3 overexpression reduced the degradation of lysosomal pathway in NDUFA10, restored the activity of mitochondrial complex I and improved mitochondrial function. Finally, our study demonstrated that CAV3 overexpression restored mitochondrial function and subsequently alleviated DCM partially through NDUFA10. The current study provides evidence that CAV3 expression is significantly downregulated in DCM. Upregulation of CAV3 interacts with NDUFA10, inhibits the degradation of lysosomal pathway in NDUFA10, a subunit of mitochondrial complex I, restores the activity of mitochondrial complex I, ameliorates mitochondrial dysfunction, and thereby protects against DCM. These findings indicate that targeting CAV3 may be a promising approach for the treatment of DCM.
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Diabetic cardiomyopathy
Apoptosis
NDUFA10
Mitochondrial dysfunction
Biomedicine
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headline:CAV3 alleviates diabetic cardiomyopathy via inhibiting NDUFA10-mediated mitochondrial dysfunction
description:The progression of diabetic cardiomyopathy (DCM) is noticeably influenced by mitochondrial dysfunction. Variants of caveolin 3 (CAV3) play important roles in cardiovascular diseases. However, the potential roles of CAV3 in mitochondrial function in DCM and the related mechanisms have not yet been elucidated. Cardiomyocytes were cultured under high-glucose and high-fat (HGHF) conditions in vitro, and db/db mice were employed as a diabetes model in vivo. To investigate the role of CAV3 in DCM and to elucidate the molecular mechanisms underlying its involvement in mitochondrial function, we conducted Liquid chromatography tandem mass spectrometry (LCâMS/MS) analysis and functional experiments. Our findings demonstrated significant downregulation of CAV3 in the cardiac tissue of db/db mice, which was found to be associated with cardiomyocyte apoptosis in DCM. Importantly, cardiac-specific overexpression of CAV3 effectively inhibited the progression of DCM, as it protected against cardiac dysfunction and cardiac remodeling associated by alleviating cardiomyocyte mitochondrial dysfunction. Furthermore, mass spectrometry analysis and immunoprecipitation assays indicated that CAV3 interacted with NDUFA10, a subunit of mitochondrial complex I. CAV3 overexpression reduced the degradation of lysosomal pathway in NDUFA10, restored the activity of mitochondrial complex I and improved mitochondrial function. Finally, our study demonstrated that CAV3 overexpression restored mitochondrial function and subsequently alleviated DCM partially through NDUFA10. The current study provides evidence that CAV3 expression is significantly downregulated in DCM. Upregulation of CAV3 interacts with NDUFA10, inhibits the degradation of lysosomal pathway in NDUFA10, a subunit of mitochondrial complex I, restores the activity of mitochondrial complex I, ameliorates mitochondrial dysfunction, and thereby protects against DCM. These findings indicate that targeting CAV3 may be a promising approach for the treatment of DCM.
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CAV3
Diabetic cardiomyopathy
Apoptosis
NDUFA10
Mitochondrial dysfunction
Biomedicine
general
Medicine/Public Health
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name:Jie Li
affiliation:
name:Tongji Medical College, Huazhong University of Science and Technology
address:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
type:PostalAddress
type:Organization
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders
address:
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
type:PostalAddress
type:Organization
name:Tingqiong Ma
affiliation:
name:Tongji Medical College, Huazhong University of Science and Technology
address:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
type:PostalAddress
type:Organization
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders
address:
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
type:PostalAddress
type:Organization
name:Man Huang
affiliation:
name:Tongji Medical College, Huazhong University of Science and Technology
address:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
type:PostalAddress
type:Organization
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders
address:
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
type:PostalAddress
type:Organization
name:Qin Fang
affiliation:
name:Tongji Medical College, Huazhong University of Science and Technology
address:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
type:PostalAddress
type:Organization
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders
address:
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
type:PostalAddress
type:Organization
email:[email protected]
name:Yan Wang
affiliation:
name:Tongji Medical College, Huazhong University of Science and Technology
address:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
type:PostalAddress
type:Organization
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders
address:
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
type:PostalAddress
type:Organization
email:[email protected]
PostalAddress:
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
name:Division of Cardiology and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
name:Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, China
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