Irisin attenuates angiotensin II-induced atrial fibrillation and atrial fibrosis via LOXL۲ and TGFβ۱/Smad۲/۳ signaling pathways

Yingbiao Wu; Jun Luo; Xiang Song; Wei Gu; Saihua Wang; Shuwen Hao; Zhiwu Dong; Zhongping Ning

Irisin attenuates angiotensin II-induced atrial fibrillation and atrial fibrosis via LOXL۲ and TGFβ۱/Smad۲/۳ signaling pathways

محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 26، شماره: 6

سال انتشار: 1402

نوع سند: مقاله ژورنالی

زبان: انگلیسی

مشاهده: 125

فایل این مقاله در 8 صفحه با فرمت PDF قابل دریافت می باشد

دریافت فایل کامل مقاله

صدور گواهی نمایه سازی
من نویسنده این مقاله هستم

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:

https://civilica.com/doc/1650680

شناسه ملی سند علمی:

JR_IJBMS-26-6_014

تاریخ نمایه سازی: 21 اردیبهشت 1402

چکیده مقاله:

Objective(s): Irisin was reported as a cardioprotective and anti-oxidative effector, while the effect on atrial fibrosis is unknown. The current research examined irisin’s function in atrial fibrillation (AF); atrial fibrosis brought on by Ang II can be suppressed, thus lessening the risk of developing AF. Materials and Methods: ۲۴۶ individuals were enrolled in the present case-control study. Chinese AF patients (n=۱۲۶), ۸۳ of whom were paroxysmal AF (PAF), ۴۳ patients with persistent AF (PeAF), and ۱۲۰ healthy controls. Saline or Ang II (۲.۰ mg/kg/day) was subcutaneously injected into healthy male C۵۷BL/۶ mice for four weeks. Once daily for four weeks, intraperitoneal injections of exogenous irisin (۵۰۰ g/kg/day) were administered. Results: In comparison to PAF patients and healthy controls (all P<۰.۰۵), PeAF patients had significantly higher rates of heart failure (HF), large left atrial size (LAD), hypertrophic protein B-type natriuretic peptide (BNP), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-۶ (IL-۶), C-terminal telopeptide of type I collagen (CTX-I), and transforming growth factor beta-۱ (TGF-β۱), while superoxide dismutase (SOD) level was low. Expression of irisin was decreased in AF patients’ serum and Ang II-infused mice. Exogenous irisin dramatically reduced apoptosis, atrial fibrosis, atrial inflammation, and the susceptibility to AF caused by Ang II. In the atrial tissue, irisin inhibited Ang II-induced fibroblast transdifferentiation, LOXL۲, TGF-β۱, collagen production, and phosphorylation of Smad۲/۳. Conclusion: The study results speculated that irisin could be a potential AF target, and it inhibited atrial fibrosis and significantly impaired increased AF susceptibility through inactivation of LOXL۲ and the TGF-β/Smad pathway.

کلیدواژه ها:

Angiotensin II ، Atrial fibrillation ، Atrial fibrosis ، Irisin ، Lysyl oxidase (LOX)-like-۲ ، Transforming growth factor-beta/Smad

نویسندگان

Yingbiao Wu