Involvement of mitochondrial fission in calcium sensing receptor-mediated vascular smooth muscle cells proliferation during hypertension

Zhang, Xin; Chen, Wen-Jia; Li, Jiawen; Qi, Shuhan; Hong, Siting; Wang, Ying; Gao, Lei; Shi, Zhiyu; Liu, Yue; Liu, Wenxiu; Chi, Yinyu; Liu, Chunnan; Fu, Yu; Yin, Xinhua

doi:10.1016/j.bbrc.2017.11.048

Cited by 9 publications

(7 citation statements)

References 17 publications

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“…Increased intravascular pressure depolarizes VSMC membrane and activates voltage-dependent calcium channels (VDCCs), leading to Ca 2+ influx [ 54 ]. In addition, the activation of calcium pathway has been proved to promote VSMC proliferation and migration in many studies [ 55 , 56 ]. Therefore, regulating the calcium signaling pathway may be one of the important therapeutic means for female AVF.…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in Arteriovenous Fistula Failure: Insights from Bioinformatics Analysis

Guo

et al. 2022

JCDD

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(1) Background: Arteriovenous fistulas (AVFs) are the preferred access for hemodialysis. Unfortunately, about 60% of patients, especially female patients, fail to receive normal dialysis within one year after surgery because of AVF failure. However, the underlying mechanisms caused by sex differences in AVF failure remain unclear. (2) Methods: We performed analysis of DEGs and functional analysis with the dataset GSE119296 to reveal the biology underlying AVF failure. Immune responses were calculated using CIBERSORT. A protein–protein interaction network and hub gene were constructed using STRING and stepwise identification of potential drugs was performed online. (3) Results: Functional analysis showed that extracellular matrix reprogramming and PI3K-AKT pathway enrichment were significant in both male and female patients. COL1A1 was the hub gene in male patients, whereas CDK1 was the hub gene in female patients. Immune responses including γδ-T cells and mast cells are activated in female patients while no significant differences were noted in the male group. (4) Conclusions: In this study, we used a series of mature and recognized bioinformatic strategies to determine the following items: (1) Reveal the pathogenesis of AVF failure through HUB genes and signaling pathways between the different sexes. (2) Determine the relationship between sex differences in AVF failure and immune abnormalities. (3) Search for relevant sex-specific drugs targeting AVF failure.

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Section: Discussionmentioning

confidence: 99%

Sex Differences in Arteriovenous Fistula Failure: Insights from Bioinformatics Analysis

Guo

et al. 2022

JCDD

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“…However, a later study demonstrated that NPS 2143 failed to increase the blood pressure in the presence of calcium channel inhibitor and type 1 Ang II receptor antagonist [36]. Our previous study has reported that the level of blood pressure in SHRs was decreased by inhibiting CaSR and mitochondrial fission [37]. In line with our findings, study was performed recently and found that elevation of the blood pressure and endothelium-independent relaxation were observed with the loss of CaSR-mediated contraction in VMSCs in the aorta and mesenteric artery in response to KCl and phenylephrine in SM22A CaSR △flox/△flox mice [14].…”

Section: Discussionmentioning

confidence: 99%

NLRP3 Inflammasome Is Involved in Calcium-Sensing Receptor-Induced Aortic Remodeling in SHRs

Zhang

Hong

et al. 2019

Mediators of Inflammation

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Increasing evidence suggests that the NLRP3 (nucleotide oligomerization domain-like receptor family, pyrin domain containing 3) inflammasome participates in cardiovascular diseases. However, its role and activation mechanism during hypertension remains unclear. In this study, we tested the role and mechanism of calcium-sensing receptor (CaSR) in NLRP3 inflammasome activation during hypertension. We observed that the expressions of CaSR and NLRP3 were increased in spontaneous hypertensive rats (SHRs) along with aortic fibrosis. In vascular smooth muscle cells (VSMCs), the activation of NLRP3 inflammasome associated with CaSR and collagen synthesis was induced by angiotensin II (Ang II). Furthermore, inhibition of CaSR and NLRP3 inflammasome attenuated proinflammatory cytokine release, suggesting that CaSR-mediated activation of the NLRP3 inflammasome may be a therapeutic target in aortic dysfunction and vascular inflammatory lesions.

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“…et al, 2016 ). Activation of CaSR has been reported to be involved in the development of various cardiovascular diseases including cardiac hypertrophy and apoptosis ( Schepelmann et al, 2016 ; Paquot et al, 2017 ; Zhang et al, 2018 ), but the molecular mechanism of the involvement of CaSR activation in heart failure has not yet been clarified and thus needs to be further explored. In the present study, we investigated the role of CaSR activation in cardiac hypertrophy and apoptosis and the relationship between CaSR and Ca 2+ -dependent CaMKII and CaN signaling pathways both in vivo and in vitro .…”

Section: Discussionmentioning

confidence: 99%

Calcium Sensing Receptor-Related Pathway Contributes to Cardiac Injury and the Mechanism of Astragaloside IV on Cardioprotection

Lü

Leng

He³

et al. 2018

Front. Pharmacol.

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Activation of calcium sensing receptor (CaSR) contributes to cardiac injury, but the underlying mechanism has not yet been examined. Astragaloside IV (AsIV) was previously reported to exhibit protective effects against various myocardial injuries. The aim of the present study was to investigate the underlying mechanism of CaSR in cardiac hypertrophy and apoptosis and to evaluate whether the protective effect of AsIV against myocardial injury is associated with CaSR and its related signaling pathway. In vivo and in vitro myocardial injury was induced by isoproterenol (Iso) or GdCl3 (a CaSR agonist) in rats and heart H9C2 cells. Cardiac cell hypertrophy, apoptosis, function, Mitochondrial Membrane Potential (MMP), mitochondrial ultrastructure, and [Ca2+]i, as well as the protein expression of CaSR, calcium/calmodulin-dependent protein kinase II (CaMKII), calcineurin (CaN), sarcoplasmic reticulum Ca2+-ATPase2a (SERCA2a), and the inositol 1,4,5-trisphosphate receptor (IP3R), were measured in vivo and/or in vitro. The results showed that AsIV attenuated cardiac hypertrophy and apoptosis and attenuated impairments in cardiac function, mitochondrial structure, and MMP induced by Iso or GdCl3 in rat myocardial tissue and H9C2 cells. Importantly, AsIV treatment inhibited the enhancement of [Ca2+]i and CaSR expression induced by Iso or GdCl3, an effect similar to that of the CaSR antagonist NPS2143. In addition, AsIV treatment repressed CaSR, CaMKII, and CaN activation and inhibited NFAT-3 nuclear translocation. Mechanistic analysis using lentivirus infection showed that CaSR overexpression activated the CaMKII and CaN signaling pathways and that this response was enhanced by Iso. The results suggested that CaSR-mediated changes in [Ca2+]i and CaMKII and CaN signaling pathways contribute to cardiac hypertrophy and apoptosis and are involved in the protective effect of astragaloside IV against cardiac injury.

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Involvement of mitochondrial fission in calcium sensing receptor-mediated vascular smooth muscle cells proliferation during hypertension

Cited by 9 publications

References 17 publications

Sex Differences in Arteriovenous Fistula Failure: Insights from Bioinformatics Analysis

Sex Differences in Arteriovenous Fistula Failure: Insights from Bioinformatics Analysis

NLRP3 Inflammasome Is Involved in Calcium-Sensing Receptor-Induced Aortic Remodeling in SHRs

Calcium Sensing Receptor-Related Pathway Contributes to Cardiac Injury and the Mechanism of Astragaloside IV on Cardioprotection

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