ReviewNature reviews. Molecular cell biology2013
Molecular basis of physiological heart growth: fundamental concepts and new players.
Review in Nature reviews. Molecular cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 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
304 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Meta-Analysis Approach to Gene Regulatory Network Inference Identifies Key Regulators of Cardiovascular Diseases.International journal of molecular sciences · 2024Pooled it
- Hepatic ChREBP Drives Cardiac Remodeling via ApoM Non-transcriptional Repression.Circulation research · 2026Article
- Glutamine Metabolism in Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2026Review
- A modelling study of right ventricular growth with valvular regurgitation.Biomechanics and modeling in mechanobiology · 2026Article
- Exercise ModulatesInternational journal of molecular sciences · 2026Article
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- The spectrum of pregnancy-induced cardiac remodeling: transitioning from healthy adaptive hypertrophy to peripartum cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.Frontiers in physiology · 2026Article
- Development of the Cardiovascular System During Adolescence.Advances in experimental medicine and biology · 2026Review
- Physical Activity and Its Impact on Cardiometabolic Disorders.Handbook of experimental pharmacology · 2026Review
- The βCirculation research · 2025Article
- Clinically Actionable Hypertrophic Cardiomyopathy Genes in South Asian Indian Patients.Journal of the American Heart Association · 2025Article
- Effect of Long-Term Isatin Administration on Daily Physical Activity and Cardiac Performance in Female Rats.The Eurasian journal of medicine · 2025Article
- Ufmylation Suppresses Unfolded Protein Response to Prevent Peripartum Cardiomyopathy.JACC. Basic to translational science · 2025Article
- Exercise-regulated lipolysis: Its role and mechanism in health and diseases.Journal of advanced research · 2025Review
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
- Cold Exposure Exacerbates Cardiac Dysfunction in a Model of Heart Failure with Preserved Ejection Fraction in Male and Female C57Bl/6J Mice.Biomedicines · 2025Article
- Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice.Cellular and molecular life sciences : CMLS · 2025Article
- TRPV2 mediates stress resilience in mouse cardiomyocytes.Communications biology · 2025Article
244 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
3 authors.
Funding
Abstract
The heart hypertrophies in response to developmental signals as well as increased workload. Although adult-onset hypertrophy can ultimately lead to disease, cardiac hypertrophy is not necessarily maladaptive and can even be beneficial. Progress has been made in our understanding of the structural and molecular characteristics of physiological cardiac hypertrophy, as well as of the endocrine effectors and associated signalling pathways that regulate it. Physiological hypertrophy is initiated by finite signals, which include growth hormones (such as thyroid hormone, insulin, insulin-like growth factor 1 and vascular endothelial growth factor) and mechanical forces that converge on a limited number of intracellular signalling pathways (such as PI3K, AKT, AMP-activated protein kinase and mTOR) to affect gene transcription, protein translation and metabolism. Harnessing adaptive signalling mediators to reinvigorate the diseased heart could have important medical ramifications.
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.