ReviewRedox biology2020
Mitochondria dysfunction and metabolic reprogramming as drivers of idiopathic pulmonary fibrosis.
Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis 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
159 citing papers in PubMed, 1 synthesis or guideline pooled it, 251 citations in OpenAlex.
- Clinical characteristics and prognostic factors of Hermansky-Pudlak syndrome with or without pulmonary fibrosis: a systematic review.Therapeutic advances in respiratory diseasePooled it
- LC-MS/MS-Based Lipidomic Profiling Reveals the Regulatory Effect of Stemoninoamide on TGF-β1-Induced Myofibroblast Transition in HFL1 Cells.Journal of mass spectrometry : JMS · 2026Article
- Targeting alveolar type II cell dysfunction in idiopathic pulmonary fibrosis: Molecular mechanisms and emerging therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- circCACNA1D drives pulmonary fibrosis by regulating pyruvate kinase M2 dimer‑tetramer switching.International journal of molecular medicine · 2026Article
- Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.Biomedicines · 2026Review
- FGF21 in idiopathic pulmonary fibrosis: mechanistic insights, translational potential, and unresolved questions.Journal of thoracic disease · 2026Review
- Article
- Cellular Senescence: Emerging Therapeutic Target for Idiopathic Pulmonary Fibrosis Pathogenic Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2026Review
- Mitochondrial transplantation in lung diseases: From mechanisms to application prospects.Genes & diseases · 2026Review
- Supervised Home-Based Telerehabilitation for Idiopathic Pulmonary Fibrosis: A Pragmatic Service Evaluation in Routine Care with Detraining Follow-up.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- CAV1-dependent mitochondrial transfer from hucMSCs reprograms epithelial lipid metabolism to relieve pulmonary fibrosis.Stem cell research & therapy · 2026Article
- Single-cell RNA sequencing reveals immune-peritubular myoid cell crosstalk driving testicular interstitial fibrosis in idiopathic non-obstructive azoospermia.Cell & bioscience · 2026Article
- Danthron prevents pulmonary fibrosis through improving mitochondrial function by upregulating carboxylesterase 3.Respiratory research · 2026Article
- Beyond scarring: a next-generation vision for pulmonary fibrosis management.Molecular biology reports · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Elevated lactate production exacerbates PM2.5-induced pulmonary fibrosis by stabilizing TGF-β1.Journal of advanced research · 2026Article
- Vitamin D attenuates the progression of pulmonary fibrosis via inhibiting thymidine kinase 1/PFKFB3-driven glycolysis.Journal of translational medicine · 2026Article
- Integrated transcriptomic and metabolomic profiling reveals immune-metabolic crosstalk and predictive biomarkers of ligustrazine treatment response in idiopathic pulmonary fibrosis.Journal of translational medicine · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
99 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease of unknown etiology. It is characterized by deposition of extracellular matrix proteins, like collagen and fibronectin in the lung interstitium leading to respiratory failure. Our understanding of the pathobiology underlying IPF is still incomplete; however, it is accepted that aging is a major risk factor in the disease while growing evidence suggests that the mitochondria plays an important role in the initiation and progression of pulmonary fibrosis. Mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, fibroblasts, and macrophages) promoting low resilience and increasing susceptibility to activation of profibrotic responses. Here we summarize changes in mitochondrial numbers, biogenesis, turnover and associated metabolic adaptations that promote disrepair and fibrosis in the lung. Finally, we highlight new possible therapeutic approaches focused on ameliorate 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.