Evidence map›Paper›PMID 42678591›Full record

ReviewMolecular biology reports2026

Regulated cell death in autoimmune diseases: molecular mechanisms and therapeutic opportunities.

Zahra Taheri, Zeinab Zarei-Behjani, Gholamreza Daryabor, Maryam Khodaei, Fatemeh Saberi, Sepideh Ghani, Gholamhossien Darya, Zeinab Dehghan

Abstract readReview
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In one paragraph

Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Zahra TaheriDepartment of Biology and Biotechnology, University of Pavia, Pavia, Italy.
Zeinab Zarei-BehjaniDepartment of Tissue Engineering and Applied Cell Sciences, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
Gholamreza DaryaborAutoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Maryam KhodaeiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fatemeh SaberiDepartment of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Sepideh GhaniCellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gholamhossien DaryaDepartment of Comparative Biomedical Sciences, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
Zeinab DehghanAutoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. dehghan.m.zeinab@gmail.com.ORCID http://orcid.org/0000-0003-4787-1287

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases develop from a breakdown in immune tolerance and arise through complex interactions among genetic susceptibility, environmental factors, immune dysregulation, and tissue damage. Although apoptosis has traditionally been recognized as a central mechanism for maintaining immune homeostasis, increasing evidence has identified several non-classical forms of regulated cell death (RCD) that also contribute to autoimmune disease pathogenesis. These pathways include ferroptosis, pyroptosis, necroptosis, PANoptosis, NETosis, parthanatos, and cuproptosis. Unlike classical apoptosis, many of these RCD mechanisms are strongly pro-inflammatory and promote the release of damage-associated molecular patterns (DAMPs), cytokines, oxidized lipids, and autoantigens, thereby enhancing both innate and adaptive immune responses. Recent studies indicate that dysregulation of RCD pathways contributes to chronic inflammation, impaired self-tolerance, immune cell abnormalities, and progressive tissue injury in autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease, psoriasis, multiple sclerosis, sjögren's syndrome, systemic sclerosis, type 1 diabetes, ulcerative colitis, dermatomyositis, ankylosing spondylitis, Chronic Dermatitis, antiphospholipid syndrome, Nephritis, and ANCA-associated vasculitis. These pathways do not function independently but form an interconnected network with extensive molecular crosstalk and compensatory interactions that influence disease progression. This review highlights the molecular mechanisms underlying emerging RCD pathways, their cell-specific roles in autoimmune diseases, and the evidence linking their involvement to disease initiation and progression. Furthermore, it discusses current and potential therapeutic approaches targeting major regulators of ferroptosis, pyroptosis, necroptosis, PANoptosis, NETosis, cuproptosis, and parthanatos. Improved understanding of the integrated landscape of the RCD network may facilitate the discovery of novel biomarkers and support the development of innovative therapies to restore immune tolerance and control chronic inflammatory damage in autoimmune diseases.

Indexed as

Autoimmune DiseasesRegulated Cell DeathAnimalsApoptosisCuproptosisFerroptosisHumansNecroptosisPyroptosisSignal TransductionApoptosisAutoimmune DiseasesFerroptosisImmune systemImmunotoleranceRegulated Cell Death

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.