Key result
Serum ANGPTL4 concentrations were significantly decreased in AF patients, and ANGPTL4 overexpression attenuated Ang II-induced fibroblast proliferation and collagen production in vitro.
Why the study?
The study investigated the association between ANGPTL4 levels and AF prognosis, its causative effect in Ang II-induced AF, and the underlying mechanisms.
Does ANGPTL4 overexpression suppress profibrogenic functions in Ang II-induced atrial fibroblasts?
Does ANGPTL4 overexpression suppress profibrogenic functions in Ang II-induced atrial fibroblasts?
ANGPTL4 is downregulated in atrial fibrillation and its overexpression suppresses Ang II-induced profibrogenic functions in atrial fibroblasts, highlighting a potential therapeutic target.
Lower ANGPTL4 in AF may support its antifibrotic role; hypothesis-generating and requires prospective validation before clinical consideration.
Objectives: 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 IIinduced 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.
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Zhu et al. (2023) studied Atrial fibrillation (n=130). ANGPTL4 vs. Healthy group / Control cells was evaluated on Serum ANGPTL4 concentrations and fibroblast proliferation, migration, and collagen production. Serum ANGPTL4 concentrations were significantly decreased in AF patients, and ANGPTL4 overexpression attenuated Ang II-induced fibroblast proliferation and collagen production in vitro.
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