Ferroptosis, necroptosis, and pyroptosis in calcium oxalate crystal-induced kidney injury

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Kun Tang , Tao Ye , Yu He , Xiaozhuo Ba , Ding Xia , Ejun Peng , Zhiqiang Chen , Zhangqun Ye , Xiaoqi Yang
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Abstract

Kidney stones represent a highly prevalent urological disorder worldwide, with high incidence and recurrence rates. Calcium oxalate (CaOx) crystal-induced kidney injury serves as the foundational mechanism for the formation and progression of CaOx stones. Regulated cell death (RCD) such as ferroptosis, necroptosis, and pyroptosis are essential in the pathophysiological process of kidney injury. Ferroptosis, a newly discovered RCD, is characterized by its reliance on iron-mediated lipid peroxidation. Necroptosis, a widely studied programmed necrosis, initiates with a necrotic phenotype that resembles apoptosis in appearance. Pyroptosis, a type of RCD that involves the gasdermin protein, is accompanied by inflammation and immune response. In recent years, increasing amounts of evidence has demonstrated that ferroptosis, necroptosis, and pyroptosis are significant pathophysiological processes involved in CaOx crystal-induced kidney injury. Herein, we summed up the roles of ferroptosis, necroptosis, and pyroptosis in CaOx crystal-induced kidney injury. Furthermore, we delved into the curative potential of ferroptosis, necroptosis, and pyroptosis in CaOx crystal-induced kidney injury.

Abstract Image

肾结石是全球高发的泌尿系统疾病,发病率和复发率都很高。草酸钙(CaOx)晶体诱发的肾损伤是 CaOx 结石形成和发展的基本机制。在肾损伤的病理生理过程中,铁蜕变、坏死和热蜕变等调节性细胞死亡(RCD)至关重要。铁变性是一种新发现的调节性细胞死亡(RCD),其特点是依赖于铁介导的脂质过氧化。坏死(Necroptosis)是一种被广泛研究的程序性坏死,其开始时的坏死表型与细胞凋亡相似。伴随着炎症和免疫反应的还有一种涉及气化蛋白的 RCD--脓毒症。近年来,越来越多的证据表明,铁蛋白沉着、坏死和热蛋白沉着是钙氧化物晶体诱发肾损伤的重要病理生理过程。在此,我们总结了铁蜕变、坏死和热蜕变在钙氧化物晶体诱导的肾损伤中的作用。此外,我们还探讨了针对钙氧化物晶体诱导的肾损伤中的铁蜕变、坏死和热蜕变的治疗潜力。
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来源期刊
CiteScore
12.30
自引率
0.00%
发文量
218
审稿时长
32 days
期刊介绍: BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
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