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  • 1
    Online Resource
    Online Resource
    P7C3‐A20 alleviates fatty liver by shaping gut microbiota and inducing FGF21/FGF1, via the AMP‐activated protein kinase/CREB regulated transcription coactivator 2 pathway
    Wiley ; 2021
    In:  British Journal of Pharmacology Vol. 178, No. 10 ( 2021-05), p. 2111-2130
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 178, No. 10 ( 2021-05), p. 2111-2130
    Abstract: Non‐alcoholic fatty liver disease (NAFLD) is a worldwide public health problem with no established pharmacological therapy. Here, we explored the potential benefit of P7C3‐A20, a novel aminopropyl carbazole compound with neuroprotective activity, in a NAFLD model, induced in mice by a high‐fat diet (HFD). Experimental Approach C57BL/6J mice were given a HFD (42% fat content) for 16 weeks to induce NAFLD. P7C3‐A20 (20 mg·kg −1 ·day −1 ) was given by gavage for 2 weeks. Indirect calorimetry, histological analysis, immunoblotting, immunohistochemistry, and biomedical examinations were performed. Gut microbiota were determined using a 16S ribosomal RNA sequencing analysis. Key Results P7C3‐A20 treatment reduced body weight gain/adiposity, improved insulin resistance, promoted energy expenditure (O 2 consumption/CO 2 production), inhibited lipid oxidation, suppressed hepatic inflammation (Kupffer cell number and pro‐inflammatory factors), decreased necroptosis/apoptosis (receptor‐interacting protein kinase 3, cleaved caspase‐3, and TUNEL), and alleviated liver fibrosis and injury. Mechanistically, P7C3‐A20 stimulated FGF21 and FGF1 via activating liver kinase B1 (LKB1) and AMP‐activated protein kinase (AMPK), which further resulted in a reduced nuclear translocation of CREB‐regulated transcription coactivator 2 (CRTC2). In AMPKα2 knockout mice, the protection of P7C3‐A20 against HFD‐induced metabolism abnormalities and fat accumulation, as well as the elevation of blood FGF21 and FGF1, was abolished. P7C3‐A20 increased the gut microbiota species richness. Moreover, it enhanced the proportions of Akkermansia , Lactobacillus , and Prevotellaceae, while reducing the proportions of Enterobacteriaceae, Escherichia , and Parasutterella. Conclusions and Implications P7C3‐A20 increased levels of NAD+ and alleviated NAFLD through stimulating FGF21 and FGF1 in an LKB1/AMPK/CRTC2‐dependent manner and shaping gut microbiota. LINKED ARTICLES This article is part of a themed issue on Cellular metabolism and diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.10/issuetoc
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v178.10
    DOI: 10.1111/bph.15008
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2029728-2
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  • 2
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    Incorporation of Gene‐Environment Interaction Terms Improved the Predictive Accuracy of Tacrolimus Stable Dose Algorithms in Chinese Adult Renal Transplant Recipients
    Wiley ; 2019
    In:  The Journal of Clinical Pharmacology Vol. 59, No. 6 ( 2019-06), p. 890-899
    Details
    In: The Journal of Clinical Pharmacology, Wiley, Vol. 59, No. 6 ( 2019-06), p. 890-899
    Abstract: The narrow therapeutic window of tacrolimus necessitates daily monitoring and predictive algorithms based on genetic and nongenetic factors. In this study, we constructed predictive algorithms for tacrolimus stable dose in a retrospective cohort of 1045 Chinese renal transplant recipients. All patients were genotyped for CYP3A4 20230T 〉 C (rs2242480), CYP3A4 T 〉 C (rs4646437), CYP3A5 *3 6898A 〉 G (rs776746), ABCB1 129T 〉 C (rs3213619); ABCB1 c.1236C 〉 T (rs01128503), ABCB1 c.2677G 〉 T/A (rs2032582) and ABCB1 c.3435C 〉 T (rs1045642) polymorphisms, and the effects of gene‐gene and gene‐environment interactions on the predictive accuracy of algorithm were evaluated. In wild‐type CYP3A4 rs2242480 (TT) carriers, patients who took calcium channel blockers had lower tacrolimus stable doses than those without the concomitant medications ( P 〈 1 × 10 −4 ). In contrast, there was no significant difference in mutant type patients. Similarly, the tacrolimus stable doses in wild‐type CYP3A5 rs776746 carriers who had hypertension were higher than those without hypertension ( P = 4.10 × 10 −3 ). More importantly, dose‐predictive algorithms with interaction terms showed higher accuracy and better performance than those without interaction terms. Our finding suggested that wild‐type CYP3A4 rs2242480 (TT) carriers should be more cautious to take tacrolimus when they are coadministrated with calcium channel blockers, and CYP3A5 rs776746 (AA) carriers may need higher tacrolimus dosage when they are in combination with hypertension.
    Type of Medium: Online Resource
    ISSN: 0091-2700 , 1552-4604
    URL: Issue
    URL: Article
    DOI: 10.1002/jcph.v59.6
    DOI: 10.1002/jcph.1379
    RVK:
    XA 52835
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2010253-7
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  • 3
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    HINT: a novel prognostic model for patients with hepatitis B virus‐related acute‐on‐chronic liver failure
    Wiley ; 2018
    In:  Alimentary Pharmacology & Therapeutics Vol. 48, No. 7 ( 2018-10), p. 750-760
    Details
    In: Alimentary Pharmacology & Therapeutics, Wiley, Vol. 48, No. 7 ( 2018-10), p. 750-760
    Abstract: HBV‐related acute‐on‐chronic liver failure (HBV‐ACLF) deteriorates rapidly in the short term, which necessitates accurate initial clinical decision making. Aims To develop a novel prognostic score for patients with HBV‐ACLF and clarify the role of thyroid hormones in HBV‐ACLF. Methods A retrospective cohort of 635 HBV‐ACLF patients was enrolled to develop and validate a novel prognostic score for HBV‐ACLF. Additionally, a cross‐sectional cohort (n = 199) and a prospective longitudinal HBV‐ACLF cohort (n = 56) were recruited to clarify the association between thyroid hormone status and the 30‐day mortality of HBV‐ACLF. Results HINT, a novel prognostic score based on hepatic encephalopathy, INR, neutrophil count, and thyroid‐stimulating hormone (TSH) using the deriving cohort (n = 426), was significantly higher in non‐survivors than survivors (1.17 ± 2.38 vs −1.87 ± 1.26, P   〈  0.0001). The AUROC of HINT for 30‐day mortality was 0.889, which was significantly higher than that of the Child‐Pugh, MELD, CLIF‐SOFA, CLIF‐C ACLF, and COSSH‐ACLF scores (all P   〈  0.05). These results were confirmed in the validation cohort (n = 209), except that the AUROC of HINT was comparable to that of COSSH‐ACLF ( P  = 0.357). Among thyroid hormones, only the TSH level on admission was significantly lower in non‐survivors than in survivors ( P  = 0.01). During the 14‐day longitudinal observation, TSH levels increased significantly in the improvement group ( P   〈  0.001) but did not change in the deterioration or fluctuation groups, and gradually increased in survivors ( P   〈  0.001) but not in non‐survivors. Conclusions HINT, as a prognostic score for HBV‐ACLF, is simpler than and superior to the Child‐Pugh, MELD, CLIF‐SOFA, and CLIF‐C ACLF scores and at least comparable with the COSSH‐ACLF score. Sequential TSH measurements may facilitate prediction of the clinical course of ACLF.
    Type of Medium: Online Resource
    ISSN: 0269-2813 , 1365-2036
    URL: Issue
    URL: Article
    DOI: 10.1111/apt.2018.48.issue-7
    DOI: 10.1111/apt.14927
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2003094-0
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  • 4
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    Melatonin ameliorates the sleep disorder induced by surgery under sevoflurane anaesthesia in aged mice
    Wiley ; 2021
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 128, No. 2 ( 2021-02), p. 256-267
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 128, No. 2 ( 2021-02), p. 256-267
    Abstract: Post‐operative sleep disorders induce adverse effects on patients, especially the elderly, which may be associated with surgery and inhalational anaesthetics. Melatonin is a neuroendocrine regulator of the sleep‐wake cycle. In this study, we analysed the alterations of post‐operative sleep in aged melatonin‐deficient (C57BL/6J) mice, and investigated if exogenous melatonin could facilitate entrainment of circadian rhythm after laparotomy under sevoflurane anaesthesia. The results showed that laparotomy under sevoflurane anaesthesia had a greater influence on post‐operative sleep than sevoflurane alone. Laparotomy under anaesthesia led to circadian rhythm shifting forward, altered EEG power density and delta power of NREM sleep, and lengthened REM and NREM sleep latencies. In the light phase, the number of waking episodes tended to decline, and wake episode duration elevated. However, these indicators presented the opposite tendency during the dark phase. Melatonin showed significant efficacy for ameliorating the sleep disorder and restoring physiological sleep, and most of the beneficial effect of melatonin was antagonized by luzindole, a melatonin receptor antagonist.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/bcpt.v128.2
    DOI: 10.1111/bcpt.13498
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2151592-X
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  • 5
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    iTRAQ‐ and LC–MS/MS‐based quantitative proteomics reveals Pqlc2 as a potential regulator of hepatic glucose metabolism and insulin signalling pathway during fasting
    Wiley ; 2021
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 48, No. 2 ( 2021-02), p. 238-249
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 48, No. 2 ( 2021-02), p. 238-249
    Abstract: Glucose homeostasis is tightly controlled by balance between glucose production and uptake in liver tissue upon energy shortage condition. Altered glucose homeostasis contributes to the pathophysiology of metabolic disorders including diabetes and obesity. Here, we aimed to analyse the change of proteomic profile upon prolonged fasting in mice with isobaric tag for relative and absolute quantification (iTRAQ) labelling followed by liquid chromatography‐mass spectrometry (LC/MS) technology. Adult male mice were fed or fasted for 16 hours and liver tissues were collected for iTRAQ labelling followed by LC/MS analysis. A total of 322 differentially expressed proteins were identified, including 189 upregulated and 133 downregulated proteins. Bioinformatics analyses, including Gene Ontology analysis (GO), Kyoto encyclopaedia of genes and genomes analysis (KEGG) and protein‐protein interaction analysis (PPI) were conducted to understand biological process, cell component, and molecular function of the 322 differentially expressed proteins. Among 322 hepatic proteins differentially expressed between fasting and fed mice, we validated three upregulated proteins (Pqlc2, Ehhadh and Apoa4) and two downregulated proteins (Uba52 and Rpl37) by western‐blotting analysis. In cultured HepG2 hepatocellular cells, we found that depletion of Pqlc2 by siRNA‐mediated knockdown impaired the insulin‐induced glucose uptake, inhibited GLUT2 mRNA level and suppressed the insulin‐induced Akt phosphorylation. By contrast, knockdown of Pqlc2 did not affect the cAMP/dexamethasone‐induced gluconeogenesis. In conclusion, our study provides important information on protein profile change during prolonged fasting with iTRAQ‐ and LC–MS/MS‐based quantitative proteomics, and identifies Pqlc2 as a potential regulator of hepatic glucose metabolism and insulin signalling pathway in this process.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.v48.2
    DOI: 10.1111/1440-1681.13419
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2020033-X
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  • 6
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    Angiotensin‐(1‐7) mitigated angiotensin II‐induced abdominal aortic aneurysms in apolipoprotein E‐knockout mice
    Wiley ; 2020
    In:  British Journal of Pharmacology Vol. 177, No. 8 ( 2020-04), p. 1719-1734
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 177, No. 8 ( 2020-04), p. 1719-1734
    Abstract: To test the hypothesis that angiotensin‐(1‐7) [Ang‐(1‐7)] may attenuate abdominal aortic aneurysm (AAA) via inhibiting vascular inflammation, extracellular matrix degradation, and smooth muscle cell (SMC) apoptosis, an animal model of AAA was established by angiotensin II (Ang II) infusion to apolipoprotein E‐knockout (ApoE ‐/‐ ) mice. Experimental Approach All mice and cultured SMCs or macrophages were divided into control, Ang II‐treated, Ang II + Ang‐(1‐7)‐treated, Ang II + Ang‐(1‐7) + A779‐treated and Ang II + Ang‐(1‐7) + PD123319‐treated groups respectively. In vivo, aortic mechanics and serum lipids were assessed. Ex vivo, AAA were examined by histology, immunohistochemistry and zymography. Cultured cells were analysed by RT‐PCR, western blots and TUNEL assays. Key Results In vivo, Ang‐(1‐7) reduced the incidence and severity of AAA induced by Ang II infusion, by inhibiting macrophage infiltration, attenuating expression of IL‐6, TNF‐α, CCL2 and MMP2, and decreasing SMC apoptosis in abdominal aortic tissues. Addition of A779 or PD123319 reversed Ang‐(1‐7)‐mediated beneficial effects on AAA. In vitro, Ang‐(1‐7) decreased expression of mRNA for IL‐6, TNF‐α, and CCL2 induced by Ang II in macrophages. In addition, Ang‐(1‐7) suppressed apoptosis and MMP2 expression and activity in Ang II‐treated SMCs. These effects were accompanied by inhibition of the ERK1/2 signalling pathways via Ang‐(1‐7) stimulation of Mas and AT 2 receptors. Conclusion and Implications Ang‐(1‐7) treatment attenuated Ang II‐induced AAA via inhibiting vascular inflammation, extracellular matrix degradation, and SMC apoptosis. Ang‐(1‐7) may provide a novel and promising approach to the prevention and treatment of AAA.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v177.8
    DOI: 10.1111/bph.14906
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 7
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    Targeting ferroptosis in cardio‐metabolic‐diseases: Mechanisms and therapeutic prospects
    Wiley ; 2023
    In:  Medicinal Research Reviews Vol. 43, No. 3 ( 2023-05), p. 683-712
    Details
    In: Medicinal Research Reviews, Wiley, Vol. 43, No. 3 ( 2023-05), p. 683-712
    Abstract: Cardio‐metabolic‐diseases (cardio‐metabolic‐diseases) are leading causes of death and disability worldwide and impose a tremendous burden on whole society as well as individuals. As a new type of regulated cell death (RCD), ferroptosis is distinct from several classical types of RCDs such as apoptosis and necroptosis in cell morphology, biochemistry, and genetics. The main molecular mechanisms of ferroptosis involve iron metabolism dysregulation, mitochondrial malfunction, impaired antioxidant capacity, accumulation of lipid‐related peroxides and membrane disruption. Within the past few years, mounting evidence has shown that ferroptosis contributes to the pathophysiological process in cardio‐metabolic‐diseases. However, the exact roles and underlying molecular mechanisms have not been fully elucidated. This review comprehensively summarizes the mechanism of ferroptosis in the development and progression of cardio‐metabolic‐diseases, so as to provide new insights for cardio‐metabolic‐diseases pathophysiology. Moreover, we highlight potential druggable molecules in ferroptosis signaling pathway, and discuss recent advances in management strategies by targeting ferroptosis for prevention and treatment of cardio‐metabolic‐diseases.
    Type of Medium: Online Resource
    ISSN: 0198-6325 , 1098-1128
    URL: Issue
    URL: Article
    DOI: 10.1002/med.v43.3
    DOI: 10.1002/med.21934
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2001841-1
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  • 8
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    Prognostic value of inflammatory and nutritional indexes among advanced NSCLC patients receiving PD ‐1 inhibitor therapy
    Wiley ; 2023
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 50, No. 2 ( 2023-02), p. 178-190
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 50, No. 2 ( 2023-02), p. 178-190
    Abstract: Though immunotherapy has to some extent improved the prognosis of patients with advanced non‐small cell lung cancer (NSCLC), only a few patients benefit. Furthermore, immunotherapy efficacy is affected by inflammatory and nutritional status of patients. To investigate whether dynamics of inflammatory and nutritional indexes were associated with prognosis, 223 patients were analysed retrospectively. The inflammatory indexes of interest were neutrophil‐to‐lymphocyte ratio (NLR), platelet‐to‐lymphocyte ratio (PLR) and systemic immune‐inflammation index (SII) while prognostic nutritional index (PNI) and the haemoglobin, albumin, lymphocyte and platelet (HALP) score were considered as nutritional indexes. Patients were divided into high and low groups or into ‘increase’ and ‘decrease’ groups based on pre‐treatment cut‐off values and index dynamics after 6‐week follow‐up respectively. High pre‐treatment PLR (OR = 2.612) and increase in NLR during follow‐up (OR = 2.516) were significantly associated with lower objective response rates. Using multivariable analysis, high pre‐treatment PLR (HR, 2.319) and increase in SII (HR, 1.731) predicted shorter progression‐free survival, while high pre‐treatment NLR (HR, 1.635), increase in NLR (HR, 1.663) and PLR (HR, 1.691) and decrease in PNI (HR, 0.611) predicted worse overall survival. The nomogram's C‐index in inside validation was 0.718 (95% CI: 0.670–0.766). Our results indicated both nutritional and inflammatory indexes are associated with survival outcomes. Inflammatory indexes were additionally linked to treatment response. Index dynamics are better predictors than baseline values in predicting survival in advanced NSCLC patients receiving PD‐1 inhibitor combined with chemotherapy as first‐line.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.v50.2
    DOI: 10.1111/1440-1681.13740
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2020033-X
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  • 9
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    Astaxanthin attenuates hepatic damage and mitochondrial dysfunction in non‐alcoholic fatty liver disease by up‐regulating the FGF21/PGC‐1α pathway
    Wiley ; 2020
    In:  British Journal of Pharmacology Vol. 177, No. 16 ( 2020-08), p. 3760-3777
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 177, No. 16 ( 2020-08), p. 3760-3777
    Abstract: Non‐alcoholic fatty liver disease (NAFLD) is considered to be one of the most common chronic liver diseases across worldwide. Astaxanthin (Ax) is a carotenoid, and beneficial effects of astaxanthin, including anti‐oxidative, anti‐inflammatory, and anti‐tumour activity, have been identified. The present study aimed to elucidate the protective effect of astaxanthin against NAFLD and its underlying mechanism. Experimental Approach Mice were fed either a high fat or chow diet, with or without astaxanthin, for up to 12 weeks. L02 cells were treated with free fatty acids combined with different doses of astaxanthin for 48 h. Histopathology, expression of lipid metabolism, inflammation, apoptosis, and fibrosis‐related gene expression were assessed. And the function of mitochondria was also evaluated. Key Results The results indicated that astaxanthin attenuated HFD‐ and FFA‐induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Astaxanthin up‐regulated FGF21 and PGC‐1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of astaxanthin on ameliorating NAFLD. Conclusion and Implications Astaxanthin attenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by up‐regulating FGF21/PGC‐1α pathway. Our results suggest that astaxanthin may become a promising drug to treat or relieve NAFLD.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v177.16
    DOI: 10.1111/bph.15099
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2029728-2
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  • 10
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    Piezo1 channel activation stimulates ATP production through enhancing mitochondrial respiration and glycolysis in vascular endothelial cells
    Wiley ; 2023
    In:  British Journal of Pharmacology Vol. 180, No. 14 ( 2023-07), p. 1862-1877
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 180, No. 14 ( 2023-07), p. 1862-1877
    Abstract: Piezo1 channels are mechanosensitive cationic channels that are activated by mechanical stretch or shear stress. Endothelial Piezo1 activation by shear stress caused by blood flow induces ATP release from endothelial cells; however, the link between shear stress and endothelial ATP production is unclear. Experimental Approach The mitochondrial respiratory function of cells was measured by using high‐resolution respirometry system Oxygraph‐2k. The intracellular Ca 2+ concentration was evaluated by using Fluo‐4/AM and mitochondrial Ca 2+ concentration by Rhod‐2/AM. Key Results The specific Piezo1 channel activator Yoda1 or its analogue Dooku1 increased [Ca 2+ ] i in human umbilical vein endothelial cells (HUVECs), and both Yoda1 and Dooku1 increased mitochondrial oxygen consumption rates (OCRs) and mitochondrial ATP production in HUVECs and primary cultured rat aortic endothelial cells (RAECs). Knockdown of Piezo1 inhibited Yoda1‐ and Dooku1‐induced increases of mitochondrial OCRs and mitochondrial ATP production in HUVECs. The shear stress mimetics, Yoda1 and Dooku1, and the Piezo1 knock‐down technique also demonstrated that Piezo1 activation increased glycolysis in HUVECs. Chelating extracellular Ca 2+ with EGTA or chelating cytosolic Ca 2+ with BAPTA‐AM did not affect Yoda1‐ and Dooku1‐induced increases of mitochondrial OCRs and ATP production, but chelating cytosolic Ca 2+ inhibited Yoda1‐ and Dooku1‐induced increase of glycolysis. Confocal microscopy showed that Piezo1 channels are present in mitochondria of endothelial cells, and Yoda1 and Dooku1 increased mitochondrial Ca 2+ in endothelial cells. Conclusion and Implications Piezo1 channel activation stimulates ATP production through enhancing mitochondrial respiration and glycolysis in vascular endothelial cells, suggesting a novel role of Piezo1 channel in endothelial ATP production.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v180.14
    DOI: 10.1111/bph.16050
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2029728-2
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