Background: Renal fibrosis is a frequent pathway leading to end-stage kidney dysfunction. In addition, renal fibrosis is the ultimate manifestation of chronic kidney diseases (CKD). Long noncoding RNAs (lncRNAs) are known to be involved in occurrence of renal fibrosis, and lncRNA plasmacytoma variant translocation 1 (PVT1) has been reported to act as a key biomarker in renal diseases. However, the role of PVT1 in renal fibrosis remains unclear. Materials and Methods: HK-2 cells were treated with TGF-β1 to mimic renal fibrosis in vitro. Gene and protein expressions in HK-2 cells were measured by qRT-PCR and Western-blot, respectively. ELISA was used to test the level of creatinine (CR) and blood urea nitrogen (BUN) in serum of mice. Additionally, unilateral ureteral obstruction (UUO)-induced renal fibrosis mice model was established to investigate the effect of PVT1 on renal fibrosis in vivo. Results: PVT1 was upregulated in TGF-β1-treated HK-2 cells. In addition, TGF-β1-induced upregulation of α-SMA and fibronectin in HK-2 cells was significantly reversed by PVT1 knockdown. Meanwhile, PVT1 bound to miR-181a-5p in HK-2 cells. Moreover, miR-181a-5p directly targeted TGF-βR1. Furthermore, miR-181a-5p antagonist could significantly reverse the antifibrotic effect of PVT1 knockdown. Besides, knockdown of PVT1 notably attenuated the symptom of renal fibrosis in vivo. Conclusion: Knockdown of PVT1 significantly inhibited the progression of renal fibrosis in vitro and in vivo. Thus, PVT1 may serve as a potential target for the treatment of renal fibrosis.
Recurrent miscarriage (RM) affects approximately 1%–5% of couples worldwide. Due to its complicated etiologies, the treatments for RM also vary greatly, including surgery for anatomic factors such as septate uterus and uterine adhesions, thyroid modulation drugs for hyperthyroidism and hypothyroidism, and aspirin and low molecular weight heparin for antiphospholipid syndrome. However, these treatment modalities are still insufficient to solve RM. Omega‐3 fatty acids are reported to modulate the dysregulation of immune cells, oxidative stress, endocrine disorders, inflammation, etc., which are closely associated with the pathogenesis of RM. However, there is a lack of a systematic description of the involvement of omega‐3 fatty acids in treating RM, and the underlying mechanisms are also not clear. In this review, we sought to determine the potential mechanisms that are highly associated with the pathogenesis of RM and the regulation of omega‐3 fatty acids on these mechanisms. In addition, we also highlighted the direct and indirect clinical evidence of omega‐3 fatty acid supplements to treat RM, which might encourage the application of omega‐3 fatty acids to treat RM, thus improving pregnancy outcomes.
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