ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Post-translational regulation of PGC-1α modulates fibrotic repair.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05976217 (Safety and Efficacy of Venetoclax in Idiopathic Pulmonary Fibrosis), which is not on this map. Cited by 14 papers.
What it found
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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.
Safety and Efficacy of Venetoclax in Idiopathic Pulmonary Fibrosis
Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanosignaling promotes macrophage apoptosis resistance in pulmonary fibrosisbioRxiv : the preprint server for biology · 2026Article
- [Research progress on the mechanism of mitochondrial dynamics in diabetic foot ulcers and its related intervention strategies].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2026Review
- Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- HDGF Protects Retinal Pigment Epithelium from Glyoxal-Induced Ferroptosis via SIRT1/PGC-1α/Nrf2 Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Targeting S1PR2 in Sepsis, One Fragmented Mitochondrion at a Time.American journal of respiratory cell and molecular biology · 2025Article
- The PERK/ATF4 pathway is required for metabolic reprogramming and progressive lung fibrosis.JCI insight · 2025Article
- The Crucial Role of the PPAR Signaling Pathway in the Diagnosis and Treatment of Chronic Obstructive Pulmonary Disease: An Analysis of Gene Expression and Macrophage Polarization.International journal of chronic obstructive pulmonary disease · 2025Article
- The Potential Role of Cigarette Smoke, Elastic Fibers, and Secondary Lung Injury in the Transition of Pulmonary Emphysema to Combined Pulmonary Fibrosis and Emphysema.International journal of molecular sciences · 2024Article
- Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024Review
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- Myeloid Heterogeneity Mediates Acute Exacerbations of Pulmonary Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Review
- The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Post-translational regulation of PGC-1α modulates fibrotic repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease associated with mitochondrial oxidative stress. Mitochondrial reactive oxygen species (mtROS) are important for cell homeostasis by regulating mitochondrial dynamics. Here, we show that IPF BAL cells exhibited increased mitochondrial biogenesis that is, in part, due to increased nuclear expression of peroxisome proliferator-activated receptor-ɣ (PPARɣ) coactivator (PGC)-1α. Increased PPARGC1A mRNA expression directly correlated with reduced pulmonary function in IPF subjects. Oxidant-mediated activation of the p38 MAPK via Akt1 regulated PGC-1α activation to increase mitochondrial biogenesis in monocyte-derived macrophages. Demonstrating the importance of PGC-1α in fibrotic repair, mice harboring a conditional deletion of Ppargc1a in monocyte-derived macrophages or mice administered a chemical inhibitor of mitochondrial division had reduced biogenesis and increased apoptosis, and the mice were protected from pulmonary fibrosis. These observations suggest that Akt1-mediated regulation of PGC-1α maintains mitochondrial homeostasis in monocyte-derived macrophages to induce apoptosis resistance, which contributes to the pathogenesis of pulmonary fibrosis.
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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.