ReviewCell death discovery2020
Mitochondrial dysfunction in fibrotic diseases.
Review in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
131 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.
- Therapeutic effects and potential mechanisms of astragaloside IV on pulmonary fibrosis: a systematic review and meta-analysis of preclinical studies.Frontiers in pharmacology · 2025Pooled it
- Multifunctional biomaterial platforms for blocking the fibrosis process and promoting cellular restoring effects in myocardial fibrosis therapy.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Peroxiredoxins in the kidney: a Jekyll and Hyde existence in disease pathogenesis.Renal failure · 2026Review
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- CHK1 activates mitophagy to attenuate cardiac aging via inhibiting AHSA1-ubiquitination.Redox biology · 2026Article
- Herba Lysimachiae Polysaccharide-Modified Selenium Nanoparticles Alleviate Oxidative Injury in Kidney Stones via TOMM22-Regulated Mitophagy Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ameliorative effect of Nano berberine in bleomycin- induced lung fibrosis in male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- The BmCPV-derived viral small peptide vsp1S4(-) suppresses viral replication by triggering apoptosis via the ROS-JNK signalling pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- S100A9 Aggravates Cardiac Fibrosis by TLR4/PGC-1α Mediated Macrophage-Myofibroblast Crosstalk.Journal of extracellular vesicles · 2026Article
- Polystyrene Microplastics Induce Sustained Cardiovascular Redox Imbalance and Alter Mitochondrial Quality Control.Antioxidants (Basel, Switzerland) · 2026Article
- Injectable antifibrotic drug-loaded hydrogels reduce fibrosis and restore myogenesis by enhancing mitochondrial metabolism and cell mechanics in an in vitro coculture model.Materials today. Bio · 2026Article
- Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Metabolomics-guided Mechanisms of Mesenchymal Stromal Cell and Exosome Therapies in Chronic Diseases.Stem cell reviews and reports · 2026Review
- TDP-43 Dysfunction Causes Hyper-Lactate State, Increased AARS1 Expression and Enhanced Protein Lactylation.Neurotoxicity research · 2026Article
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Linezolid-mediated Prevention of Fibroblast Activation and Tissue Fibrosis via Mitochondrial Translation Inhibition.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Graphene Far-Infrared Therapy Enhances Diabetic Wound Healing Through Potential Mitigation of Oxidative Stress and Inflammation and Regulation of Chemokines and Macrophage Polarization.International journal of molecular sciences · 2026Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly oxygen-consuming organs that are sensitive to mitochondrial dysfunction. Moreover, the fibrotic process of skin and islet is closely related to mitochondrial dysfunction as well. This review summarized emerging mechanisms related to mitochondrial dysfunction in different fibrotic organs and tissues above. First, it highlighted the important elucidation of mitochondria morphological changes, mitochondrial membrane potential and structural damage, mitochondrial DNA (mtDNA) damage and reactive oxidative species (ROS) production, etc. Second, it introduced the abnormality of mitophagy and mitochondrial transfer also contributed to the fibrotic process. Therefore, with gaining the increasing knowledge of mitochondrial structure, function, and origin, we could kindle a new era for the diagnostic and therapeutic strategies of many fibrotic diseases based on mitochondrial dysfunction.
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What OpenQuestion holds
Registered trials
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.