Emerging insights into the role of ferroptosis in the pathogenesis of autoimmune diseases

Fan, Jun‐Yu; Jiang, Ting; He, Dongyi

doi:10.3389/fimmu.2023.1120519

Cited by 15 publications

(3 citation statements)

References 162 publications

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“…Recently, the role of ferroptosis in autoimmune diseases has been reviewed. Fan et al ( 11 ) highlighted crosstalk between ferroptosis and different immune cells and discussed the role of ferroptosis in autoimmune disease and Lai et al ( 10 ) also discussed how ferroptosis contributes to the pathogenesis of SLE, RA and IBD. However, the autoimmune diseases included in the aforementioned reviews are relatively limited and did not summarize the association between ferroptosis and autoimmune response.…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis: A potential therapeutic target in autoimmune disease (Review)

et al. 2023

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Ferroptosis is a distinct type of regulated cell death characterized by iron overload and lipid peroxidation. Ferroptosis is regulated by numerous factors and controlled by several mechanisms. This cell death type has a relationship with the immune system, which may be regulated by damage-associated molecular patterns. Ferroptosis participates in the progression of autoimmune diseases, including autoimmune hepatitis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, Parkinson's Disease, psoriasis and insulin-dependent diabetes mellitus. The present review summarizes the role of ferroptosis in autoimmune disorders and discusses ferroptosis as a potential therapeutic target for autoimmune disease.

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Section: Discussionmentioning

confidence: 99%

Ferroptosis: A potential therapeutic target in autoimmune disease (Review)

et al. 2023

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“…However, the study of ferroptosis offers a fresh vantage point for investigating these conditions, introducing a novel perspective into the realm of autoimmune disease research. One of the contributing factors to the development of autoimmunity is the aberrant initiation of cell death and inadequate clearance of deceased cells, leading to the exposure or release of intracellular contents that activate the immune system [ 624 ]. Ferroptosis plays a substantial role in influencing both the quantity and functionality of immune cells625.…”

Section: Ferroptosis In Pathologiesmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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“…The accumulation of ROS and lipid peroxides promotes tissue damage and bacterial dissemination, whereas HO-1 increases the levels of ferrous metals, contributing to Mtb survival [ 154 ]. Additionally, regulating ferritin and ferroportin by HO-1 can reduce intracellular oxidative stress and promote iron exit from the intracellular environment through the ferroportin protein [ 155 , 158 ]. Qiang et al showed that PtpA triggers ferroptosis to promote Mtb pathogenicity and dissemination.…”

Section: Cell Death Mechanisms Activated By Mtb Virulence Factors: Th...mentioning

confidence: 99%

Virulence Factors of Mycobacterium tuberculosis as Modulators of Cell Death Mechanisms

et al. 2023

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Mycobacterium tuberculosis (Mtb) modulates diverse cell death pathways to escape the host immune responses and favor its dissemination, a complex process of interest in pathogenesis-related studies. The main virulence factors of Mtb that alter cell death pathways are classified according to their origin as either non-protein (for instance, lipomannan) or protein (such as the PE family and ESX secretion system). The 38 kDa lipoprotein, ESAT-6 (early antigen-secreted protein 6 kDa), and another secreted protein, tuberculosis necrotizing toxin (TNT), induces necroptosis, thereby allowing mycobacteria to survive inside the cell. The inhibition of pyroptosis by blocking inflammasome activation by Zmp1 and PknF is another pathway that aids the intracellular replication of Mtb. Autophagy inhibition is another mechanism that allows Mtb to escape the immune response. The enhanced intracellular survival (Eis) protein, other proteins, such as ESX-1, SecA2, SapM, PE6, and certain microRNAs, also facilitate Mtb host immune escape process. In summary, Mtb affects the microenvironment of cell death to avoid an effective immune response and facilitate its spread. A thorough study of these pathways would help identify therapeutic targets to prevent the survival of mycobacteria in the host.

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Emerging insights into the role of ferroptosis in the pathogenesis of autoimmune diseases

Cited by 15 publications

References 162 publications

Ferroptosis: A potential therapeutic target in autoimmune disease (Review)

Ferroptosis: A potential therapeutic target in autoimmune disease (Review)

The mechanism of ferroptosis and its related diseases

Virulence Factors of Mycobacterium tuberculosis as Modulators of Cell Death Mechanisms

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