ReviewNature reviews. Cardiology2019
Mechanical regulation of gene expression in cardiac myocytes and fibroblasts.
Review in Nature reviews. Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 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
140 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.
- Pooled it
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Biofabrication for spatial control of multiscale biological crosstalk in tissue models.npj biomedical innovations · 2026Review
- A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026Review
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Peroxisomal dysfunction in cardiac adipose tissue is involved in obesity-associated cardiac hypertrophy.Journal of advanced research · 2026Article
- Rhythms of growth: unveiling the mechanobiology behind heart maturation.The Journal of physiology · 2026Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis.Nature cardiovascular research · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Spatial imprints of emergent cardiomyocyte states in the pressure-overloaded heart.bioRxiv : the preprint server for biology · 2026Article
- Restoration of structural organization in engineered cardiac microtissues is promoted by cardiomyocyte beating.Communications biology · 2026Article
- The Phoenix Heart-PICSO and the Rebirth of Embryonic Life in the Ischemic Myocardium.Journal of cardiovascular development and disease · 2026Review
- Ultrapliable bioelectronic interface for mechanosensitive cardiac electrophysiology.Science advances · 2026Article
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The intact heart undergoes complex and multiscale remodelling processes in response to altered mechanical cues. Remodelling of the myocardium is regulated by a combination of myocyte and non-myocyte responses to mechanosensitive pathways, which can alter gene expression and therefore function in these cells. Cellular mechanotransduction and its downstream effects on gene expression are initially compensatory mechanisms during adaptations to the altered mechanical environment, but under prolonged and abnormal loading conditions, they can become maladaptive, leading to impaired function and cardiac pathologies. In this Review, we summarize mechanoregulated pathways in cardiac myocytes and fibroblasts that lead to altered gene expression and cell remodelling under physiological and pathophysiological conditions. Developments in systems modelling of the networks that regulate gene expression in response to mechanical stimuli should improve integrative understanding of their roles in vivo and help to discover new combinations of drugs and device therapies targeting mechanosignalling in heart disease.
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.