ArticleCirculation2017
Fibroblast-Specific Genetic Manipulation of p38 Mitogen-Activated Protein Kinase In Vivo Reveals Its Central Regulatory Role in Fibrosis.
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Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 1 of them a synthesis that pooled it.
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199citing papers in PubMed, 1 pooled it
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199 citing papers in PubMed, 1 synthesis or guideline pooled it, 299 citations in OpenAlex.
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- The biology of PKM2 in the metabolism and senescence in diabetic kidney disease.Journal of diabetes investigation · 2026Review
- Treadmill exercise activates mechanosensitive Piezo1 to inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction in mice.Basic research in cardiology · 2026Article
- Targeting sorting nexin 3 to treat pulmonary fibrosis by dual modulating Wnt/β-catenin signaling.Cell death & disease · 2026Article
- Development of peribronchiolar fibrosis is associated with local immune and MAPK pathway activation in a murine model of deployment-related constrictive bronchiolitis.Frontiers in public health · 2026Article
- Adamts1 Exacerbates Post-Myocardial Infarction Scar Formation via Mechanosensing of Integrin α8.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Factors Released by Polarized Neutrophil-like Cells Modulate Cardiac Fibroblast Phenotype and Limit the Inflammatory Response After Myocardial Infarction.Biomedicines · 2025Article
- Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart.Circulation · 2025Article
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.Nature cardiovascular research · 2025Article
- Cell type specificity of Hippo-YAP signaling in cardiac development and disease.Journal of molecular and cellular cardiology · 2025Review
- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- The PERK-p38 MAPK Axis Drives Endoplasmic Reticulum Stress-Induced Apoptosis in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Dual inhibition of TGFβ and PDGF improves RV remodeling and function in response to RV pressure or volume-loading.Physiological reports · 2025Article
- Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward injury sites after kidney injury.iScience · 2025Article
139 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Jeffery D MolkentinFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.). jeff.molkentin@cchmc.org jendavis@uw.edu.
Darrian BuggFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Natasha GhearingFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Lisa E DornFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Peter KimFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Michelle A SargentFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Jagadambika GunajeFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Kinya OtsuFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.).
Jennifer DavisFrom Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, OH (J.D.M., N.G., L.E.D., M.A.S.); Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, OH (J.D.M); Department of Bioengineering, University of Washington, Seattle (D.B., P.K., J.G. J.D.); and Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, United Kingdom (K.O.). jeff.molkentin@cchmc.org jendavis@uw.edu.
Howard Hughes Medical Institute · USCincinnati Children's Hospital Medical Center · USUniversity of Washington · US
Funding
WNT/^-catenin Signaling and Cardiac Fibrosis P01HL069779 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI OSINSKA, HANNA · 2002 to 2017
$27.0MThrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1R01HL105924 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin · 2011 to 2026
$7.3MMolecular Pathways Controlling Cardiac Gene ExpressionR37HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 2008 to 2017
$3.8MMBNL1's function in myofibroblast transformation and fibrosisR00HL119353 · NHLBI · UNIVERSITY OF WASHINGTON · PI DAVIS, JENNIFER MICHELLE · 2015 to 2017
$747kNHLBI NIH HHS P01 HL069779NHLBI NIH HHS R00 HL119353NHLBI NIH HHS R01 HL105924NHLBI NIH HHS R37 HL060562
Abstract
backgroundIn the heart, acute injury induces a fibrotic healing response that generates collagen-rich scarring that is at first protective but if inappropriately sustained can worsen heart disease. The fibrotic process is initiated by cytokines, neuroendocrine effectors, and mechanical strain that promote resident fibroblast differentiation into contractile and extracellular matrix-producing myofibroblasts. The mitogen-activated protein kinase p38α (
methodsA conditional
resultsIn mice, loss of
conclusionsThese findings suggest that signals from diverse modes of injury converge on p38α mitogen-activated protein kinase within the fibroblast to program the fibrotic response and myofibroblast formation in vivo, suggesting a novel therapeutic approach with p38 inhibitors for future clinical application.
Indexed as
ActinsAllelesAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCells, CulturedCytokinesFibroblastsFibrosisHeart VentriclesIschemiaKidneyLungMiceMice, Inbred C57BLMice, TransgenicActinsalpha-smooth muscle actin, mouseBasic Helix-Loop-Helix ProteinsCytokinesMitogen-Activated Protein Kinase 14Tcf21 protein, mousefibroblastsfibrosismice, transgenicmitogen-activated protein kinase kinasesmyocardial infarction
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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.