ReviewJournal of cardiovascular development and disease2019
Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.
Review in Journal of cardiovascular development and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Extracellular matrix remodeling in animal models of anthracycline-induced cardiomyopathy: a meta-analysis.Journal of molecular medicine (Berlin, Germany) · 2021Pooled it
- Review
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Investigating effects of acute severe hypoxia and p38 MAPK inhibition on boldness and anxiety-like behavior in zebrafish larvae.Frontiers in behavioral neuroscience · 2026Article
- NF-Frontiers in cardiovascular medicine · 2026Review
- Lingguizhugan Decoction Attenuates Angiotensin II-Induced Cardiac Hypertrophy Through the LITAF Signaling Pathway.Combinatorial chemistry & high throughput screening · 2026Article
- Angiopoietin-like protein 7: A narrative review and its potential roles in post-myocardial infarction fibrosis.iScience · 2025Review
- Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis.Journal of cardiovascular translational research · 2025Review
- Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression.ACS omega · 2025Article
- Exploring Anti-Inflammatory Treatment as Upstream Therapy in the Management of Atrial Fibrillation.Journal of clinical medicine · 2025Review
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- Mechanism and research progress of MAPK signaling pathway in myocardial fibrosis.Frontiers in cardiovascular medicine · 2025Review
- Cardioprotective mechanism of Qixuan Yijianing formula in Graves' disease mice using miRNA sequencing approach.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Pharmacological Inhibition of P-Rex1/Rac1 Axis Blocked Angiotensin II-Induced Cardiac Fibrosis.Cardiovascular drugs and therapy · 2024Article
- A New Ex Vivo Model to Study Cardiac Fibrosis in Whole Mouse Hearts.JACC. Basic to translational science · 2024Article
- Stem cell-based therapy for fibrotic diseases: mechanisms and pathways.Stem cell research & therapy · 2024Review
- ERK3 is involved in regulating cardiac fibroblast function.Physiological reports · 2024Article
- Shared Proteins and Pathways of Cardiovascular and Cognitive Diseases: Relation to Vascular Cognitive Impairment.Journal of proteome research · 2024Article
- Gut microbiota as a residual risk factor causally influencing cardiac structure and function: Mendelian randomization analysis and biological annotation.Frontiers in microbiology · 2024Article
- Traditional Therapeutics and Potential Epidrugs for CVD: Why Not Both?Life (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cardiac fibroblast is a remarkably versatile cell type that coordinates inflammatory, fibrotic and hypertrophic responses in the heart through a complex array of intracellular and intercellular signaling mechanisms. One important signaling node that has been identified involves p38 MAPK; a family of kinases activated in response to stress and inflammatory stimuli that modulates multiple aspects of cardiac fibroblast function, including inflammatory responses, myofibroblast differentiation, extracellular matrix turnover and the paracrine induction of cardiomyocyte hypertrophy. This review explores the emerging importance of the p38 MAPK pathway in cardiac fibroblasts, describes the molecular mechanisms by which it regulates the expression of key genes, and highlights its potential as a therapeutic target for reducing adverse myocardial remodeling.
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.