ArticleCurrent opinion in physiology2022
Hippo-Yap signaling in cardiac and fibrotic remodeling.
Article in Current opinion in physiology, 2022. 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, 12 citations in OpenAlex.
- Sex-dependent epigenomic and transcriptomic reprogramming links maternal obesity to cardiac remodeling in adult offspring.American journal of physiology. Heart and circulatory physiology · 2026Article
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Fecal microbiota transplantation mitigates cardiac remodeling and functional impairment in mice with chronic colitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Dimethyl Fumarate Reverses β-Adrenoceptor-Mediated Myocardial Fibrosis in Mice by Inhibiting Yes-Associated Protein-Regulated Expression of Intermediate-Conductance CaJournal of the American Heart Association · 2026Article
- Infarct border-zone biomechanics after myocardial infarction: linking mechanotransduction, fibrosis, and ventricular dysfunction.Frontiers in bioengineering and biotechnology · 2026Review
- Targeting the NO-sGC-cGMP Pathway: Mechanisms of Action of Vericiguat in Chronic Heart Failure.Cells · 2025Review
- Crosstalk between MST1-Hippo and Wnt/β-Catenin, Notch, and PI3K/Akt pathways in cardiac physiology and pathology.Journal of physiology and biochemistry · 2025Review
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Unlocking cardiomyocyte renewal potential for myocardial regeneration therapy.Journal of molecular and cellular cardiology · 2023Review
- Rodent Models of Dilated Cardiomyopathy and Heart Failure for Translational Investigations and Therapeutic Discovery.International journal of molecular sciences · 2023Review
- Advances in the design, generation, and application of tissue-engineered myocardial equivalents.Frontiers in bioengineering and biotechnology · 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
1 author at 1 institution in 1 country.
Funding
Abstract
Cardiac injury initiates a tissue remodeling process in which aberrant fibrosis plays a significant part, contributing to impaired contractility of the myocardium and the progression to heart failure. Fibrotic remodeling is characterized by the activation, proliferation, and differentiation of quiescent fibroblasts to myofibroblasts, and the resulting effects on the extracellular matrix and inflammatory milieu. Molecular mechanisms underlying fibroblast fate decisions and subsequent cardiac fibrosis are complex and remain incompletely understood. Emerging evidence has implicated the Hippo-Yap signaling pathway, originally discovered as a fundamental regulator of organ size, as an important mechanism that modulates fibroblast activity and adverse remodeling in the heart, while also exerting distinct cell type-specific functions that dictate opposing outcomes on heart failure. This brief review will focus on Hippo-Yap signaling in cardiomyocytes, cardiac fibroblasts, and other non-myocytes, and present mechanisms by which it may influence the course of cardiac fibrosis and dysfunction.
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.