Programmed cell death in autoimmune diseases: ferroptosis.

Ann Biol Clin (Paris)

Rheumatology and Immunology Department, Haining Kanghua Hospital, No. 2299, Jiangnan Avenue, Jiaxing, China.

Published: April 2024

Ferroptosis is an iron dependent cell death driven by lipid peroxidation. Over the past decade, increasing evidence has confirmed that ferroptosis plays an irreplaceable role in the occurrence and development of many diseases, including various cancers, neurodegenerative diseases, cardiovascular diseases and autoimmune diseases. Autoimmune disease is an inflammatory disease characterized by the breakdown of immune tolerance. Nowadays, accumulating evidence indicates that ferroptosis is closely related to the pathogenesis of autoimmune diseases. Therefore, this review briefly introduced the mechanism of ferroptosis, and focused on the related research of ferroptosis in multiple autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), ankylosing spondylitis (AS). In addition, we also presented the idea of targeting ferroptosis as a potential therapeutic target for patients with autoimmune diseases, which may provide a direction for the development of new therapeutic strategies.

Download full-text PDF

Source
http://dx.doi.org/10.1684/abc.2024.1866DOI Listing

Publication Analysis

Top Keywords

autoimmune diseases
20
cell death
8
diseases
8
diseases autoimmune
8
ferroptosis
7
autoimmune
6
programmed cell
4
death autoimmune
4
diseases ferroptosis
4
ferroptosis ferroptosis
4

Similar Publications

Methotrexate-Induced Accelerated Nodulosis: A Case Series.

Mediterr J Rheumatol

December 2024

Department of Clinical Immunology and Rheumatology, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, India.

Methotrexate-induced nodulosis, also known as methotrexate-induced accelerated nodulosis (MIAN), is a rare side effect of methotrexate therapy. Methotrexate (MTX) is commonly used to treat various autoimmune diseases, such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. In this case series, we present patients with MIAN, discussing their clinical features, diagnostic approaches, and management strategies.

View Article and Find Full Text PDF

Systematically generating differential diagnoses facilitates a clinician's history, physical exam, and clinical evaluation. is an acronym for pathophysiologies to consider in a differential diagnosis: immune reactions and dysregulation, metabolic, psychiatric, allergic, structural, social, infectious, vascular, endocrine/exocrine, degenerative, iatrogenic, congenital, traumatic, autoimmune, toxic, idiopathic, neoplastic, and genetic. We suggest that this mnemonic includes several improvements on previous pathophysiology-based acronyms and have informally validated this new mnemonic with two lists of common diseases.

View Article and Find Full Text PDF

Biological sex is closely associated with the properties and extent of the immune response, with males and females showing different susceptibilities to diseases and variations in immunity. Androgens, predominantly in males, generally suppress immune responses, while estrogens, more abundant in females, tend to enhance immunity. It is also established that sex hormones at least partially explain sex biases in different diseases, particularly autoimmune diseases in females.

View Article and Find Full Text PDF

Background: Chronic Nonbacterial Osteomyelitis (CNO) is a rare auto-inflammatory disease that mainly affects children, and manifests with single or multiple painful bone lesions. Due to the lack of specific laboratory markers, CNO diagnosis is a matter of exclusion from different conditions, first and foremost bacterial osteomyelitis and malignancies. Whole Body Magnetic Resonance (WBMR) and bone biopsy are the gold standard for the diagnosis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!