创伤和缺氧后的脂肪组织功能障碍会增加手术后粘连的风险:治疗干预的潜力。

Rozita Khodashahi, Mahmoud Tavakkoli, Gorgon A Ferns, Leyla Feyzmohammadi, Amir Hossein Mirzaei, Mohsen Aliakbarian, Mohammad-Hassan Arjmand
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引用次数: 0

摘要

手术后粘连是一项医学难题,尤其是在腹部和盆腔手术后。这是指妇科腔道或腹腔内结缔组织形成的纤维化疤痕。手术损伤和缺氧导致的脂肪组织(AT)功能失调会通过不同的分子机制增加手术后粘连的风险。手术创伤和缺氧过程中产生的损伤相关分子模式(DAMPs)和缺氧诱导因子 1α(HIF-1α)会诱发脂肪组织功能障碍,从而促进炎症、氧化应激、代谢改变和组织坏死通路,导致手术后粘连。HIF-1α和DAMPs可被视为治疗靶点,以防止腹部或盆腔手术肥胖患者的AT功能障碍并减少粘连的形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Adipose Tissue Dysfunction Following Trauma and Hypoxia Increases the Risk of Post-Surgical Adhesion: Potential for Therapeutic Interventions

Post-surgical adhesion is a medical challenge, especially following abdominal and pelvic surgeries. This refers to the formation of fibrotic scars that form from connective tissue in the gynecological tract or abdominal cavity. Dysfunctional adipose tissue (AT) by surgical injuries and hypoxia increases the risk of post-surgical adhesion through different molecular mechanisms. Damage-associated molecular patterns (DAMPs) and Hypoxia-induced factor 1 alpha (HIF-1α) produced during surgery trauma and hypoxia induce AT dysfunction to promote inflammation, oxidative stress, metabolic alterations, and profibrotic pathways, which contribute to post-surgical adhesions. HIF-1α and DAMPs can be considered therapeutic targets to prevent AT dysfunction and diminish the formation of adhesions in obese patients undergoing abdominal or pelvic surgeries.

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