ReviewFrontiers in cell and developmental biology2025
Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed.
- CHK1 activates mitophagy to attenuate cardiac aging via inhibiting AHSA1-ubiquitination.Redox biology · 2026Article
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Corisin induces proteostasis stress to drive epithelial injury and pulmonary fibrosis.Nature communications · 2026Article
- Article
- Cellular Senescence: Emerging Therapeutic Target for Idiopathic Pulmonary Fibrosis Pathogenic Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2026Review
- Combination of Ophiopogonin D, Ginsenoside Rg1, and Ginsenoside Rg3 ameliorates idiopathic pulmonary fibrosis via inhibiting type 2 alveolar epithelial cell senescence and epithelial-mesenchymal transition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Fibrosis suppressive effect and mechanism of CaSR positive allosteric modulators/p-dioxanone copolymers.Drug delivery and translational research · 2026Article
- Neutralization of Microbiota-Derived Corisin Shows Early Amelioration of Advanced Pulmonary Fibrosis.Advances in respiratory medicine · 2026Article
- Multiomics Reveals Mitochondrial and Metabolic Perturbations Underlying Cyclotriphosphazene-Induced Lung Injury.Environment & health (Washington, D.C.) · 2026Article
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Multi-omics integration identifies APOE as a metabolic regulator of macrophage-fibroblast crosstalk in idiopathic pulmonary fibrosis.Frontiers in immunology · 2026Article
- Immunosenescence in Idiopathic Pulmonary Fibrosis.Journal of inflammation research · 2026Review
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Hesperetin Alleviates Bleomycin-Induced Pulmonary Fibrosis by Modulating Cellular Senescence and Promoting Impaired Autophagy in a CISD2-Dependent Manner.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with an unknown origin and complex pathogenic mechanisms. A deeper understanding of these mechanisms is essential for effective treatment. Pulmonary fibrosis is associated with the senescence of alveolar type II epithelial (ATⅡ) cells. Additionally, ATⅡ senescence can lead to a senescence-associated secretory phenotype, which affects cellular communication and disrupts lung tissue repair, contributing to the development of IPF. The role of mitochondrial dysfunction in senescence-related diseases is increasingly recognized. It can induce ATⅡ senescence through apoptosis, impaired autophagy, and disrupted energy metabolism, potentially playing a key role in IPF progression. This article explores the therapeutic potential of targeting cellular senescence and mitochondrial dysfunction, emphasizing their significant roles in IPF pathogenesis.
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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.