Ferritinophagy: Molecular mechanisms and role in disease

IF 2.9 4区 医学 Q2 PATHOLOGY
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引用次数: 0

Abstract

Ferritinophagy is a regulatory pathway of iron homeostasis. It is a process in which nuclear receptor coactivator 4 (NCOA4) carries ferritin to autophagolysosomes for degradation. After ferritin is degraded by autophagy, iron ions are released, which promotes the labile iron pool (LIP) to drive the Fenton reaction to cause lipid peroxidation. Furthermore, ferroptosis promoted by the accumulation of lipid reactive oxygen species (ROS) induced by ferritinophagy can cause a variety of systemic diseases. In clinical studies, targeting the genes regulating ferritinophagy can prevent and treat such diseases. This article describes the key regulatory factors of ferritinophagy and the mechanism of ferritinophagy involved in ferroptosis. It also reviews the damage of ferritinophagy to the body, providing a theoretical basis for further finding clinical treatment methods.

噬铁蛋白:分子机制和在疾病中的作用
铁蛋白吞噬是铁平衡的一种调节途径。在这一过程中,核受体辅激活子 4(NCOA4)将铁蛋白带到自噬溶酶体中进行降解。铁蛋白被自噬降解后,铁离子被释放出来,从而促进易变铁池(LIP)驱动芬顿反应,导致脂质过氧化。此外,由铁蛋白吞噬诱导的脂质活性氧(ROS)积累所促进的铁变态反应可导致多种系统性疾病。在临床研究中,靶向调控噬铁蛋白的基因可以预防和治疗这类疾病。本文介绍了噬铁蛋白的关键调控因子和噬铁蛋白参与铁蛋白沉积的机制。文章还回顾了噬铁蛋白对机体的损害,为进一步寻找临床治疗方法提供了理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.00
自引率
3.60%
发文量
405
审稿时长
24 days
期刊介绍: Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist''s practice.
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