دورية أكاديمية
أعرض في EDS

Irisin attenuates vascular remodeling in hypertensive mice induced by Ang II by suppressing Ca 2+ -dependent endoplasmic reticulum stress in VSMCs.

التفاصيل البيبلوغرافية
العنوان: Irisin attenuates vascular remodeling in hypertensive mice induced by Ang II by suppressing Ca 2+ -dependent endoplasmic reticulum stress in VSMCs.
المؤلفون: Li RL; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China.; Sichuan Key Laboratory of TCM Regulating Metabolic Diseases, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, 610072, PR China., Zhuo CL; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Yan X; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Li H; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Lin L; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Li LY; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Jiang Q; West China College of Preclinical Medicine and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, PR China., Zhang D; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Wang XM; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Liu LL; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China.; West China College of Preclinical Medicine and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, PR China., Huang WJ; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Wang YL; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Li XY; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Mao Y; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Chen Y; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Liu X; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Xu QC; Department of Biomedical Engineering, Southern University of Science and Technology, Guangdong 518055, PR. China., Cai YY; Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Yang XJ; Core Facilities, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Chen HY; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China.; Core Facilities, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Wu SS; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China.; Core Facilities, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China., Jiang W; Molecular Medicine Research Center, State Key Laboratory of Biotherapy,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China.
المصدر: International journal of biological sciences [Int J Biol Sci] 2024 Jan 01; Vol. 20 (2), pp. 680-700. Date of Electronic Publication: 2024 Jan 01 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Ivyspring International Country of Publication: Australia NLM ID: 101235568 Publication Model: eCollection Cited Medium: Internet ISSN: 1449-2288 (Electronic) Linking ISSN: 14492288 NLM ISO Abbreviation: Int J Biol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Lake Haven, N.S.W., Australia : Ivyspring International, c2004-
مواضيع طبية MeSH: Angiotensin II*/metabolism , Hypertension*, Mice ; Male ; Animals ; Fibronectins/metabolism ; AMP-Activated Protein Kinases/metabolism ; Vascular Remodeling ; Calcium/metabolism ; Muscle, Smooth, Vascular/metabolism ; Endoplasmic Reticulum Stress
مستخلص: Vascular remodeling plays a vital role in hypertensive diseases and is an important target for hypertension treatment. Irisin, a newly discovered myokine and adipokine, has been found to have beneficial effects on various cardiovascular diseases. However, the pharmacological effect of irisin in antagonizing hypertension-induced vascular remodeling is not well understood. In the present study, we investigated the protection and mechanisms of irisin against hypertension and vascular remodeling induced by angiotensin II (Ang II). Adult male mice of wild-type, FNDC5 (irisin-precursor) knockout, and FNDC5 overexpression were used to develop hypertension by challenging them with Ang II subcutaneously in the back using a microosmotic pump for 4 weeks. Similar to the attenuation of irisin on Ang II-induced VSMCs remodeling, endogenous FNDC5 ablation exacerbated, and exogenous FNDC5 overexpression alleviated Ang II-induced hypertension and vascular remodeling. Aortic RNA sequencing showed that irisin deficiency exacerbated intracellular calcium imbalance and increased vasoconstriction, which was parallel to the deterioration in both ER calcium dysmetabolism and ER stress. FNDC5 overexpression/exogenous irisin supplementation protected VSMCs from Ang II-induced remodeling by improving endoplasmic reticulum (ER) homeostasis. This improvement includes inhibiting Ca 2+ release from the ER and promoting the re-absorption of Ca 2+ into the ER, thus relieving Ca 2+ -dependent ER stress. Furthermore, irisin was confirmed to bind to its receptors, αV/β5 integrins, to further activate the AMPK pathway and inhibit the p38 pathway, leading to vasoprotection in Ang II-insulted VSMCs. These results indicate that irisin protects against hypertension and vascular remodeling in Ang II-challenged mice by restoring calcium homeostasis and attenuating ER stress in VSMCs via activating AMPK and suppressing p38 signaling.
Competing Interests: Competing Interests: The authors have declared that no competing interest exists.
(© The author(s).)
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فهرسة مساهمة: Keywords: Calcium homeostasis; ERS; Hypertension; Irisin; Vascular remodeling
المشرفين على المادة: 11128-99-7 (Angiotensin II)
0 (Fibronectins)
EC 2.7.11.31 (AMP-Activated Protein Kinases)
SY7Q814VUP (Calcium)
0 (FNDC5 protein, mouse)
تواريخ الأحداث: Date Created: 20240103 Date Completed: 20240105 Latest Revision: 20240306
رمز التحديث: 20240306
مُعرف محوري في PubMed: PMC10758105
DOI: 10.7150/ijbs.84153
PMID: 38169582
قاعدة البيانات: MEDLINE
الوصف
تدمد:1449-2288
DOI:10.7150/ijbs.84153