ArticleInternational journal of molecular medicine2019
Crosstalk between mitogen-activated protein kinase inhibitors and transforming growth factor-β signaling results in variable activation of human dermal fibroblasts.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Fibroblasts in Scar Formation: Biology and Clinical Translation.Oxidative medicine and cellular longevity · 2022Pooled it
- Advances in pharmacotherapy for fibrotic interstitial lung disease.Medical review (2021) · 2026Review
- Allicin Attenuates Silica-Induced Pulmonary Fibrosis by Targeting the Serpinb2/NF-κB Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Recent advances on anti-scarring properties of amniotic membrane: emerging strategies and clinical potentials in regenerative medicine.Stem cell research & therapy · 2026Review
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
- Modulation of renal fibrosis-related signaling pathways by traditional Chinese medicine: molecular mechanisms and experimental evidence.International urology and nephrology · 2025Review
- The Versatile Role of Peroxisome Proliferator-Activated Receptors in Immune-Mediated Intestinal Diseases.Cells · 2024Review
- Non-immune factors cause prolonged myofibroblast phenotype in implanted synthetic heart valve scaffolds.Applied materials today · 2024Article
- The Role of Transforming Growth Factor-β (TGF-β) in Asthma and Chronic Obstructive Pulmonary Disease (COPD).Cells · 2024Review
- Crosstalk between CAFs and tumour cells in head and neck cancer.Cell death discovery · 2024Review
- Myogenic Anti-Nucleolin Aptamer iSN04 Inhibits Proliferation and Promotes Differentiation of Vascular Smooth Muscle Cells.Biomolecules · 2024Article
- AESIS-1, a Rheumatoid Arthritis Therapeutic Peptide, Accelerates Wound Healing by Promoting Fibroblast Migration in a CXCR2-Dependent Manner.International journal of molecular sciences · 2024Article
- Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024Article
- Revisited and innovative perspectives of oral ulcer: from biological specificity to local treatment.Frontiers in bioengineering and biotechnology · 2024Review
- Extracellular matrix stiffness-The central cue for skin fibrosis.Frontiers in molecular biosciences · 2023Review
- Differential Effects of Toll-Like Receptor Activation and Differential Mediation by MAP Kinases of Immune Responses in Microglial Cells.Cellular and molecular neurobiology · 2022Article
- First study on the effect of transforming growth factor beta 1 and insulin-like growth factor 1 on the chondrogenesis of elephant articular chondrocytes in a scaffold-based 3D culture model.Veterinary world · 2022Article
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- AITC inhibits fibroblast-myofibroblast transition via TRPA1-independent MAPK and NRF2/HO-1 pathways and reverses corticosteroids insensitivity in human lung fibroblasts.Respiratory research · 2021Article
- Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics.Acta pharmaceutica Sinica. B · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast activation is a key step in the establishment of skin fibrosis induced by acute injury, and it is characterized by the differentiation of plastic resident tissue fibroblasts into contractile, extracellular matrix‑secreting myofibroblasts. As fibroblast activation must be regulated in vivo, fibroblasts receive signals from the surrounding environment that initiate their fibrotic program. Thus, the present study investigated the effects of mitogen‑activated protein kinase (MAPK) signaling pathways on fibroblast activation. It was demonstrated in primary human dermal fibroblasts that small molecule‑mediated inhibition of extracellular signal‑regulated kinase (ERK) and c‑Jun N‑terminal kinase (JNK) potentiated fibroblast activation, and that small molecule‑mediated inhibition of p38 antagonized fibroblast activation. ERK and JNK inhibition cooperatively enhanced fibroblast activation mediated by treatment with exogenous transforming growth factor (TGF)‑β1, and p38 inhibition antagonized ERK inhibitor‑mediated or JNK inhibitor‑mediated fibroblast activation. Transcript analysis demonstrated that ERK and JNK inhibitor‑mediated fibroblast activation was accompanied by distinct changes in the expression of TGF‑β‑associated ligands and receptors, and that p38 inhibitor‑mediated antagonism of fibroblast activation was accompanied by a distinct expression paradigm of TGF‑β‑associated genes, including upregulation of betaglycan. ERK inhibitor‑mediated and JNK inhibitor‑mediated fibroblast activation was partially antagonized by small molecule‑mediated inhibition of TGF‑β receptor (R)1, indicating that these mechanisms of fibroblast activation are partially dependent on TGF‑β/TGF‑βR signaling. These data collectively demonstrate and provide partial explanations of the varied effects and pathway dependencies of MAPK inhibitor‑mediated effects on fibroblast activation.
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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.