TY - JOUR ID - 21999 TI - ANGPTL4 suppresses the profibrogenic functions of atrial fibroblasts induced by angiotensin II by up-regulating PPARγ JO - Iranian Journal of Basic Medical Sciences JA - IJBMS LA - en SN - 2008-3866 AU - Zhu, Xi AU - Zhang, Xiaogang AU - Gu, Wei AU - Zhao, Hanjun AU - Hao, Shuwen AU - Ning, Zhongping AD - Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital (Shanghai Health Medical College Affiliated Zhoupu Hospital) shanghai 201318, China AD - Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital (Shanghai Health Medical College Affiliated Zhoupu Hospital) shanghai 201318, ChinaEmail: ningzpsh@163.com Tel: +86-021-68135590. Y1 - 2023 PY - 2023 VL - 26 IS - 5 SP - 587 EP - 593 KW - Atrial fibrillation KW - Atrial fibrosis KW - Lipoprotein lipase KW - Peroxisome proliferator-activated receptor-γ KW - Triglyceride DO - 10.22038/ijbms.2023.69196.15077 N2 - Objective(s): The present study’s objective was to investigate the association between angiopoietin-like 4 (ANGPTL4) levels and the prognosis of Atrial fibrillation (AF), the causative effect in angiotensin II- (Ang II) induced AF, and its underlying mechanisms.Materials and Methods: Baseline serum ANGPTL-4 concentrations were measured in 130 patients with AF. Rat atrial fibroblasts were isolated from 14-day-old SD rats and transfected with Ang II treatment. Transfected cells were divided into: The control group, ANGPTL4-OE group, Ang II group, and Ang II+ANGPTL4-OE group. Transfected cells were used to analyze fibroblasts’ proliferation, migration, and collagen production at the cellular level. RT-qPCR and western blotting evaluated the ANGPTL4-targeted gene and PPARγ-Akt pathway.Results: In patients with AF, serum ANGPTL4 concentrations decreased significantly compared with the healthy group. ANGPTL4 mRNA and protein expressions were significantly down-regulated in Ang II-induced cardiac fibroblasts. ANGPTL4 overexpression potentially attenuated Ang II‑induced fibroblast proliferation, migration, and collagen production in atrial tissue. ANGPTL4 inhibited the signaling proteins, such as PPARγ, α-SMA, and Akt.Conclusion: Our experimental data speculate that ANGPTL4 is a key factor in regulating AF progression. Therefore, increasing ANGPTL4 expression could be an effective strategy for AF treatment.v UR - https://ijbms.mums.ac.ir/article_21999.html L1 - https://ijbms.mums.ac.ir/article_21999_5627278764f8fdd9f9f0539664990d35.pdf ER -