ArticleActa pharmacologica Sinica2021
Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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17 citing papers in PubMed, 45 citations in OpenAlex.
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- Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026Review
- A Single-Cell Transcriptomic Atlas Elucidates a Microglial Gene Signature Linking Ferroptosis to Mitochondrial Dysfunction in Epilepsy.Journal of inflammation research · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Whole-genome sequencing reveals genetic structure and adaptive genes in Nepalese buffalo breeds.BMC genomics · 2024Article
- SENP1-Mediated HSP90ab1 DeSUMOylation in Cardiomyocytes Prevents Myocardial Fibrosis by Paracrine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The potential roles of stress-induced phosphoprotein 1 and connexin 43 in rats with reperfusion arrhythmia.Immunity, inflammation and disease · 2023Article
- Extracellular Vesicles and Cx43-Gap Junction Channels Are the Main Routes for Mitochondrial Transfer from Ultra-Purified Mesenchymal Stem Cells, RECs.International journal of molecular sciences · 2023Article
- Mitochondrial Connexins and Mitochondrial Contact Sites with Gap Junction Structure.International journal of molecular sciences · 2023Review
- Modulation of the mTOR Pathway by Curcumin in the Heart of Septic Mice.Pharmaceutics · 2022Article
- mTORC2/RICTOR exerts differential levels of metabolic control in human embryonic, mesenchymal and neural stem cells.Protein & cell · 2022Article
- Article
- Secretion of miRNA-326-3p by senescent adipose exacerbates myocardial metabolism in diabetic mice.Journal of translational medicine · 2022Article
- Mitochondrial transfer/transplantation: an emerging therapeutic approach for multiple diseases.Cell & bioscience · 2022Review
- Functional implications of neutrophil metabolism during ischemic tissue repair.Current opinion in pharmacology · 2022Review
- Connexin 43 in Mitochondria: What Do We Really Know About Its Function?Frontiers in physiology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rictor is a key component of the mammalian target of rapamycin complex 2 (mTORC2) and is required for Akt phosphorylation (Ser473). Our previous study shows that knockdown of Rictor prevents cardiomyocyte differentiation from mouse embryonic stem (ES) cells and induces abnormal electrophysiology of ES cell-derived cardiomyocytes (ESC-CMs). Besides, knockdown of Rictor causes down-expression of connexin 43 (Cx43), the predominant gap junction protein, that is located in both the sarcolemma and mitochondria in cardiomyocytes. Mitochondrial Cx43 (mtCx43) plays a crucial role in mitochondrial function. In this study, we used the model of cardiomyocyte differentiation from mouse ES cells to elucidate the mechanisms for the mitochondrial damage in ESC-CMs after knockdown of Rictor. We showed swollen and ruptured mitochondria were observed after knockdown of Rictor under transmission electron microscope. ATP production and mitochondrial transmembrane potential were significantly decreased in Rictor-knockdown cells. Furthermore, knockdown of Rictor inhibited the activities of mitochondrial respiratory chain complex. The above-mentioned changes were linked to inhibiting the translocation of Cx43 into mitochondria by knockdown of Rictor. We revealed that knockdown of Rictor inactivated the mTOR/Akt signalling pathway and subsequently decreased HDAC6 expression, resulted in Hsp90 hyper-acetylation caused by HDAC6 inhibition, thus, inhibited the formation of Hsp90-Cx43-TOM20 complex. In conclusion, the mitochondrial Cx43 participates in shRNA-Rictor-induced mitochondrial function damage in the ESC-CMs.
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