ReviewThe Journal of clinical investigation2017
Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis.
Review in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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
145 citing papers in PubMed, 227 citations in OpenAlex.
- Engineered levothyroxine dry powder for inhalation to treat idiopathic pulmonary fibrosis.Drug delivery and translational research · 2026Article
- Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.Biomedicines · 2026Review
- Article
- Mitochondrial-derived microproteins in lung disease: insights and implications.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Decreased Complex I Activity in Blood lymphocytes Correlates with Idiopathic Pulmonary Fibrosis Severity.Biochemical genetics · 2026Article
- Emerging role of the immunoproteasome as a druggable target in lung inflammatory diseases.Respiratory research · 2026Review
- Age-related mitochondrial energy metabolism reprogramming occurs in granulosa cells during ovarian aging.Frontiers in endocrinology · 2026Observational
- Mitophagy in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- Aging-associated transcriptional programming of mitochondrial respiration in alveolar type II epithelial cells.Frontiers in cell and developmental biology · 2026Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Epithelial damage and ageing: the perfect storm.Thorax · 2025Review
- Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice.Nature communications · 2025Article
- Tissue Fibrosis Decoded via Cellular Senescence: Mechanisms, Treatments, and Emerging Technologies.Aging and disease · 2025Review
- A Simple Ratio in a Complex Disease: Exploring the Neutrophil-to-Lymphocyte Ratio in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Hyperoxia-induced senescence in fetal airway smooth muscle cells: role of mitochondrial reactive oxygen species and endoplasmic reticulum stress.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Mitochondrial Unfolded Protein Response (mtUPR) Activation Improves Pathological Alterations in Cellular Models of Ethylmalonic Encephalopathy.Antioxidants (Basel, Switzerland) · 2025Article
- The critical role of mitophagy in cell senescence-mediated pulmonary fibrosis and potential therapeutic strategies.Molecular biology reports · 2025Review
85 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized by abnormal scarring of the lung parenchyma. There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence. These divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-related diseases such as IPF. Therapeutic approaches that target aging processes may be beneficial for halting the progression of disease and improving quality of life in IPF patients.
Indexed as
Identifiers
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.