ArticleScientific reports2021
Sensitization of the UPR by loss of PPP1R15A promotes fibrosis and senescence in IPF.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- Aregs-IGFBP3-mediated SMC-like cells apoptosis impairs beige adipocytes formation in aged mice.Molecular metabolism · 2025Article
- Integrating bulk and single-cell RNA sequencing data: unveiling RNA methylation and autophagy-related signatures in chronic obstructive pulmonary disease patients.Scientific reports · 2025Article
- Identification of mitochondria-related genes associated with anesthetics in patients undergoing off-pump coronary artery bypass grafting surgery.Frontiers in surgery · 2025Article
- GDF15 antagonism limits severe heart failure and prevents cardiac cachexia.Cardiovascular research · 2024Article
- Article
- Single-cell resolution of human airway epithelial cells exposed to bronchiolitis obliterans-associated chemicals.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Exploring Co-expression Modules-Traits Correlation through Weighted Gene Co-expression Network Analysis: A Promising Approach in Wound Healing Research.Medical journal of the Islamic Republic of Iran · 2024Article
- Article
- HSP47: A Therapeutic Target in Pulmonary Fibrosis.Biomedicines · 2023Review
- IL-8 concurrently promotes idiopathic pulmonary fibrosis mesenchymal progenitor cell senescence and PD-L1 expression enabling escape from immune cell surveillance.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Single-cell protein activity analysis reveals a novel subpopulation of chondrocytes and the corresponding key master regulator proteins associated with anti-senescence and OA progression.Frontiers in immunology · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
The unfolded protein response (UPR) is a direct consequence of cellular endoplasmic reticulum (ER) stress and a key disease driving mechanism in IPF. The resolution of the UPR is directed by PPP1R15A (GADD34) and leads to the restoration of normal ribosomal activity. While the role of PPP1R15A has been explored in lung epithelial cells, the role of this UPR resolving factor has yet to be explored in lung mesenchymal cells. The objective of the current study was to determine the expression and role of PPP1R15A in IPF fibroblasts and in a bleomycin-induced lung fibrosis model. A survey of IPF lung tissue revealed that PPP1R15A expression was markedly reduced. Targeting PPP1R15A in primary fibroblasts modulated TGF-β-induced fibroblast to myofibroblast differentiation and exacerbated pulmonary fibrosis in bleomycin-challenged mice. Interestingly, the loss of PPP1R15A appeared to promote lung fibroblast senescence. Taken together, our findings demonstrate the major role of PPP1R15A in the regulation of lung mesenchymal cells, and regulation of PPP1R15A may represent a novel therapeutic strategy in IPF.
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.