ArticleInternational journal of molecular sciences2021
Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Targeting the DNA damage repair protein RAD51 alters fibroblast metabolism and enhances apoptosis in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- A Novel Wogonin Derivative Induces Apoptosis in PC-3M Cells by Targeting Mitochondrial Dysfunction and Activating the ROS-p38/MAPK Pathway.Molecules (Basel, Switzerland) · 2026Article
- Mitochondrial proteomics reveals reductive metabolism dependent on glutamine in fibroblasts of idiopathic pulmonary fibrosis under hypoxia.Scientific reports · 2026Article
- Intracristal space proteome mapping using super-resolution proximity labeling with isotope-coded probes.Nature communications · 2025Article
- Apoptosis in spotted sea bass brain and astroglia-like cell line implies a possible pathogenesis of Lateolabrax maculatus iridovirus infection.Fish physiology and biochemistry · 2025Article
- PGC-1 alpha regulates mitochondrial biogenesis to promote silica-induced pulmonary fibrosis.Toxicology research · 2025Article
- The Mechanism of a Novel Mitochondrial-Targeted Icaritin Derivative in Regulating Apoptosis of BEL-7402 Cells Based on the SIRT3 and CypD-Mediated ROS/p38 MAPK Signaling Pathway.Molecules (Basel, Switzerland) · 2025Article
- Dexmedetomidine ameliorates hepatic ischemia reperfusion injury via modulating SIRT3 mediated mitochondrial quality control.Scientific reports · 2025Article
- The unmet promise: a critical review of antioxidant strategies in myocardial ischemia-reperfusion injury and the path towards precision medicine.Frontiers in pharmacology · 2025Review
- HCMV strain- and cell type-specific alterations in membrane contact sites point to the convergent regulation of organelle remodeling.Journal of virology · 2024Article
- Article
- Treprostinil Reconstitutes Mitochondrial Organisation and Structure in Idiopathic Pulmonary Fibrosis Cells.International journal of molecular sciences · 2023Article
- Article
- Mitochondrial Oxidative Metabolism: An Emerging Therapeutic Target to Improve CKD Outcomes.Biomedicines · 2023Review
- Antiproliferative Mechanisms of a Polyphenolic Combination of Kaempferol and Fisetin in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
- Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts.International journal of molecular sciences · 2023Review
- Wild-type S100A3 and S100A13 restore calcium homeostasis and mitigate mitochondrial dysregulation in pulmonary fibrosis patient-derived cells.Frontiers in cell and developmental biology · 2023Article
- Effect of Hypoxia in the Transcriptomic Profile of Lung Fibroblasts from Idiopathic Pulmonary Fibrosis.Cells · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by increased activation of fibroblasts/myofibroblasts. Previous reports have shown that IPF fibroblasts are resistant to apoptosis, but the mechanisms remain unclear. Since inhibition of the mitochondrial permeability transition pore (mPTP) has been implicated in the resistance to apoptosis, in this study, we analyzed the role of mitochondrial function and the mPTP on the apoptosis resistance of IPF fibroblasts under basal conditions and after mitomycin C-induced apoptosis. We measured the release of cytochrome c, mPTP opening, mitochondrial calcium release, oxygen consumption, mitochondrial membrane potential, ADP/ATP ratio, ATP concentration, and mitochondrial morphology. We found that IPF fibroblasts were resistant to mitomycin C-induced apoptosis and that calcium, a well-established activator of mPTP, is decreased as well as the release of pro-apoptotic proteins such as cytochrome c. Likewise, IPF fibroblasts showed decreased mitochondrial function, while mPTP was less sensitive to ionomycin-induced opening. Although IPF fibroblasts did not present changes in the mitochondrial membrane potential, we found a fragmented mitochondrial network with scarce, thinned, and disordered mitochondria with reduced ATP levels. Our findings demonstrate that IPF fibroblasts are resistant to mitomycin C-induced apoptosis and that altered mPTP opening contributes to this resistance. In addition, IPF fibroblasts show mitochondrial dysfunction evidenced by a decrease in respiratory parameters.
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