Current pharmaceutical biotechnology · 2026
OX-LDL Drives Excessive Autophagy and Apoptosis of Trophoblasts by the ROS/mTOR/NLRP3 Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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He Fengping, Xiong Chuanyin, Chen Lujing, Lou Jiwu, Meng Lin, Jiang Xueqing, Song Linhe, Zhang Yongmei, Yan Tizhen
Аннотация
INTRODUCTION: Unexplained recurrent spontaneous abortion (uRSA) is a devastating clinical condition that affects 2-6% of pregnancies, and more than 50% of cases remain without an identified cause despite comprehensive evaluation, resulting in a significant emotional and reproductive burden for patients. This study clarifies a novel molecular mechanism linking oxidized low-density lipoprotein (OX-LDL)-induced oxidative stress to trophoblast dysfunction through the ROS/mTOR/NLRP3 signaling pathway and identifies miRNA-146 as a key negative regulator with therapeutic potential.
METHODS: The human trophoblast cell line HTR8/SVneo and decidual tissues from patients with uRSA and controls were analyzed using MTT assays, TUNEL staining, ROS detection, Western blotting, qRT-PCR, and immunohistochemistry. miRNA-146 mimics and inhibitors were applied to investigate the regulatory mechanisms.
RESULTS: Exposure to OX-LDL significantly increased ROS production and upregulated mTOR and NLRP3 expression, leading to excessive autophagy and apoptosis in trophoblast cells. miRNA- 146 negatively regulated this pathway, restoring cell viability and migration. Clinical samples from uRSA patients showed decreased miRNA-146 expression and increased mTOR and NLRP3 expression in decidual tissues.
DISCUSSION: These findings demonstrate a mechanistic link between OX-LDL-induced oxidative stress and trophoblast dysfunction in uRSA. miRNA-146 counteracts these effects by inhibiting the ROS/mTOR/NLRP3 signaling axis.
CONCLUSION: miRNA-146 mitigates OX-LDL-induced trophoblast autophagy and apoptosis and may represent a potential therapeutic target for uRSA.
METHODS: The human trophoblast cell line HTR8/SVneo and decidual tissues from patients with uRSA and controls were analyzed using MTT assays, TUNEL staining, ROS detection, Western blotting, qRT-PCR, and immunohistochemistry. miRNA-146 mimics and inhibitors were applied to investigate the regulatory mechanisms.
RESULTS: Exposure to OX-LDL significantly increased ROS production and upregulated mTOR and NLRP3 expression, leading to excessive autophagy and apoptosis in trophoblast cells. miRNA- 146 negatively regulated this pathway, restoring cell viability and migration. Clinical samples from uRSA patients showed decreased miRNA-146 expression and increased mTOR and NLRP3 expression in decidual tissues.
DISCUSSION: These findings demonstrate a mechanistic link between OX-LDL-induced oxidative stress and trophoblast dysfunction in uRSA. miRNA-146 counteracts these effects by inhibiting the ROS/mTOR/NLRP3 signaling axis.
CONCLUSION: miRNA-146 mitigates OX-LDL-induced trophoblast autophagy and apoptosis and may represent a potential therapeutic target for uRSA.