ReviewInternational journal of molecular sciences2021
Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis.
Review 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 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Ceramide-Driven Mechanisms in Pulmonary Fibrosis.Metabolites · 2026Review
- Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis.Respiratory research · 2026Article
- Article
- Advances in JNK inhibitor development: therapeutic prospects in neurodegenerative diseases and fibrosis.Archives of pharmacal research · 2025Review
- The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025Review
- hAMSCs regulate EMT in the progression of experimental pulmonary fibrosis through delivering miR-181a-5p targeting TGFBR1.Stem cell research & therapy · 2025Article
- Citrullinated and malondialdehyde-acetaldehyde-modified fibrinogen activates macrophages and promotes profibrotic responses in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Adiponectin suppresses stiffness-dependent, profibrotic activation of lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK.Biomolecules · 2024Review
- MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.The Journal of clinical investigation · 2024Article
- Small-Molecule Activation of Protein Phosphatase 2A Counters Bleomycin-Induced Fibrosis in Mice.ACS pharmacology & translational science · 2023Article
- Alvespimycin Exhibits Potential Anti-TGF-β Signaling in the Setting of a Proteasome Activator in Rats with Bleomycin-Induced Pulmonary Fibrosis: A Promising Novel Approach.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Reversal of Pulmonary Fibrosis: Human Umbilical Mesenchymal Stem Cells from Wharton's Jelly versus Human-Adipose-Derived Mesenchymal Stem Cells.International journal of molecular sciences · 2023Article
- Review
- GWAS on Imputed Whole-Genome Sequence Variants Reveal Genes Associated with Resistance toGenes · 2022Article
- Shared mechanisms and crosstalk of COVID-19 and osteoporosis via vitamin D.Scientific reports · 2022Article
- GANE can Improve Lung Fibrosis by Reducing Inflammation via Promoting p38MAPK/TGF-β1/NF-κB Signaling Pathway Downregulation.ACS omega · 2022Article
- Systematic Analysis Strategy Based on Network Pharmacology to Investigate the Potential Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Pro-Inflammatory Serum Amyloid a Stimulates Renal Dysfunction and Enhances Atherosclerosis in Apo E-Deficient Mice.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is one of the most symptomatic progressive fibrotic lung diseases, in which patients have an extremely poor prognosis. Therefore, understanding the precise molecular mechanisms underlying pulmonary fibrosis is necessary for the development of new therapeutic options. Stress-activated protein kinases (SAPKs), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38) are ubiquitously expressed in various types of cells and activated in response to cellular environmental stresses, including inflammatory and apoptotic stimuli. Type II alveolar epithelial cells, fibroblasts, and macrophages are known to participate in the progression of pulmonary fibrosis. SAPKs can control fibrogenesis by regulating the cellular processes and molecular functions in various types of lung cells (including cells of the epithelium, interstitial connective tissue, blood vessels, and hematopoietic and lymphoid tissue), all aspects of which remain to be elucidated. We recently reported that the stepwise elevation of intrinsic p38 signaling in the lungs is correlated with a worsening severity of bleomycin-induced fibrosis, indicating an importance of this pathway in the progression of pulmonary fibrosis. In addition, a transcriptome analysis of RNA-sequencing data from this unique model demonstrated that several lines of mechanisms are involved in the pathogenesis of pulmonary fibrosis, which provides a basis for further studies. Here, we review the accumulating evidence for the spatial and temporal roles of SAPKs in 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.