[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Tan, Ying; Xia, Fengfan; Li, Lulan; Peng, Xiaojie; Liu, Wenqian; Zhang, Yaoyuan; Fang, Haihong; Zeng, Zhenhua; Chen, Zhongqing

doi:10.1155/2021/6669075

Cited by 17 publications

(13 citation statements)

References 95 publications

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“… 96 − 100 The fusion of the mitochondrial membrane includes the outer membrane fusion, which is induced by mitofusin 1 (MFN1) and mitofusin 2 (MFN2), and the inner membrane fusion induced by optic atrophy 1 (OPA1). 99 , 100 It was reported that MFN1 and MFN2 are localized on the OMM and ER membrane and exist as homo- or heterodimers that function to induce the membrane fusion of mitochondria. 101 , 102 It has also been reported that these GTPases function to construct mitochondria-ER tethering sites for Ca 2+ transport.…”

Section: Results and Discussionmentioning

confidence: 99%

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

et al. 2022

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We previously reported that a cyclometalated iridium (Ir) complex-peptide hybrid (IPH) 4 functionalized with a cationic KKKGG peptide unit on the 2-phenylpyridine ligand induces paraptosis, a relatively newly found programmed cell death, in cancer cells (Jurkat cells) via the direct transport of calcium (Ca 2+ ) from the endoplasmic reticulum (ER) to mitochondria. Here, we describe that CGP37157, an inhibitor of a mitochondrial sodium (Na + )/Ca 2+ exchanger, induces paraptosis in Jurkat cells via intracellular pathways similar to those induced by 4 . The findings allow us to suggest that the induction of paraptosis by 4 and CGP37157 is associated with membrane fusion between mitochondria and the ER, subsequent Ca 2+ influx from the ER to mitochondria, and a decrease in the mitochondrial membrane potential ( ΔΨ m ). On the contrary, celastrol, a naturally occurring triterpenoid that had been reported as a paraptosis inducer in cancer cells, negligibly induces mitochondria-ER membrane fusion. Consequently, we conclude that the paraptosis induced by 4 and CGP37157 (termed paraptosis II herein) proceeds via a signaling pathway different from that of the previously known paraptosis induced by celastrol, a process that negligibly involves membrane fusion between mitochondria and the ER (termed paraptosis I herein).

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Section: Results and Discussionmentioning

confidence: 99%

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

et al. 2022

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“…The increased fusion or decreased fission promotes the formation of an extended mitochondrial network, and the decreased fusion or increased fission leads to the fragmentation of mitochondria [39]. The imbalance of mitochondrial fusion and fission played a key role in the mechanism for myocardial injury in diabetes mellitus [10,40]; mitochondrial dysfunction seems to be an important target for therapy to improve 14 Oxidative Medicine and Cellular Longevity cardiac function directly [41]. After abnormal glycolipid exposures, we observed that the mitochondrial membrane potential and intracellular ATP concentration were reduced.…”

Section: Discussionmentioning

confidence: 99%

SFRP2 Improves Mitochondrial Dynamics and Mitochondrial Biogenesis, Oxidative Stress, and Apoptosis in Diabetic Cardiomyopathy

Huang

Zheng

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. The mitochondrial dynamics and mitochondrial biogenesis are essential for maintaining the bioenergy function of mitochondria in diabetic cardiomyopathy (DCM). Previous studies have revealed that secreted frizzled-related protein 2 (SFRP2) is beneficial against apoptosis and oxidative stress. However, no research has confirmed whether SFRP2 regulates oxidative stress and apoptosis through mitochondrial function in DCM. Methods. Exposure of H9C2 cardiomyocytes in high glucose (HG) 25 mM and palmitic acid (PAL) 0.2 mM was used to simulate DCM in vitro. H9C2 cells with SFRP2 overexpression or SFRP2 knockdown were constructed and cultured under glucolipotoxicity or normal glucose conditions. An SD rat model of type 2 diabetes mellitus (T2DM) was generated using a high-fat diet combined with a low-dose STZ injection. Overexpression of SFRP2 in the rat model was generated by using an adeno-associated virus approach. CCK-8, TUNEL assay, and DHE staining were used to detect cell viability, and MitoTracker Red CMXRos was used to detect changes in mitochondrial membrane potential. We used qRT-PCR and western blot to further explore the mechanisms of SFRP2 regulating mitochondrial dynamics through the AMPK/PGC1-α pathway to improve diabetic cardiomyocyte injury. Results. Our results indicated that SFRP2 was significantly downregulated in H9C2 cells and cardiac tissues in T2DM conditions, accompanied by decreased expression of mitochondrial dysfunction. The mitochondrial membrane potential was reduced, and the cells were led to oxidative stress injury and apoptosis. Furthermore, the overexpression of SFRP2 could reverse apoptosis and promote mitochondrial function in T2DM conditions in vitro and in vivo. We also found that silencing endogenous SFRP2 could further promote glucolipotoxicity-induced mitochondrial dysfunction and apoptosis in cardiomyocytes, accompanied by downregulation of p-AMPK. Conclusion. SFRP2 exerted cardioprotective effects by salvaging mitochondrial function in an AMPK-PGC1-α-dependent manner, which modulates mitochondrial dynamics and mitochondrial biogenesis, reducing oxidative stress and apoptosis. SFRP2 may be a promising therapeutic biomarker in DCM.

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“…Dysfunctions in mitochondrial dynamics have a central role in the development of AKI and cardiovascular diseases, since excessive fission and low fusion are detrimental to both tissues [ 9 , 55 , 56 ]. A large number of studies indicated that OPA1 and Mfn 2 may suffer post-transcriptional and translational modifications, reducing their expression in kidney diseases [ 57 , 58 , 59 , 60 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C

Neres-Santos

Junho

Panico

et al. 2021

Cells

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Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular changes. Mitochondrial dysfunction and oxidative and nitrosative stress have been reported in the pathophysiology of CRS3. It is known that vitamin C, an antioxidant, has proven protective capacity for cardiac, renal, and vascular endothelial tissues. Therefore, the present study aimed to assess whether vitamin C provides protection to heart and the kidneys in an in vivo CRS3 model. The unilateral renal ischemia and reperfusion (IR) protocol was performed for 60 min in the left kidney of adult mice, with and without vitamin C treatment, immediately after IR or 15 days after IR. Kidneys and hearts were subsequently collected, and the following analyses were conducted: renal morphometric evaluation, serum urea and creatinine levels, high-resolution respirometry, amperometry technique for NO measurement, gene expression of mitochondrial dynamic markers, and NOS. The analyses showed that the left kidney weight was reduced, urea and creatinine levels were increased, mitochondrial oxygen consumption was reduced, NO levels were elevated, and Mfn2 expression was reduced after 15 days of IR compared to the sham group. Oxygen consumption and NO levels in the heart were also reduced. The treatment with vitamin C preserved the left kidney weight, restored renal function, reduced NO levels, decreased iNOS expression, elevated constitutive NOS isoforms, and improved oxygen consumption. In the heart, oxygen consumption and NO levels were improved after vitamin C treatment, whereas the three NOS isoforms were overexpressed. These data indicate that vitamin C provides protection to the kidneys and some beneficial effects to the heart after IR, indicating it may be a preventive approach against cardiorenal insults.

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[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Cited by 17 publications

References 95 publications

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

SFRP2 Improves Mitochondrial Dynamics and Mitochondrial Biogenesis, Oxidative Stress, and Apoptosis in Diabetic Cardiomyopathy

Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C

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[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Cited by 17 publications

References 95 publications

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca2+Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca2+Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

SFRP2 Improves Mitochondrial Dynamics and Mitochondrial Biogenesis, Oxidative Stress, and Apoptosis in Diabetic Cardiomyopathy

Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C

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Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum

Induction of Paraptosis by Cyclometalated Iridium Complex-Peptide Hybrids and CGP37157 via a Mitochondrial Ca²⁺Overload Triggered by Membrane Fusion between Mitochondria and the Endoplasmic Reticulum