ReviewNature reviews. Cardiology2018
Mechanisms of physiological and pathological cardiac hypertrophy.
Review in Nature reviews. Cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 942 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
942 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,600 citations in OpenAlex.
- Circadian rhythm disruption in cardiovascular disease: a systematic review and meta-analysis of mechanistic evidence from animal models.BMC medicine · 2026Pooled it
- Cardiomyocyte-enriched OTUD5 alleviates pathological myocardial hypertrophy by deubiquitinating STAT3 and modulating the STAT3-PGC-1α axis.Experimental & molecular medicine · 2026Article
- Tetraethylammonium-Sensitive ventricular repolarization in diabetic rat myocardium: effects of rosiglitazone.Archives of endocrinology and metabolism · 2026Article
- RMND1 dysfunction causes OXPHOS deficiency and alters mitoribosomal protein homeostasis in vivo.EMBO molecular medicine · 2026Article
- E3 Ubiquitin Ligase UBR5 Aggravates Cardiac Hypertrophy Via Inhibiting Nrf2/HO-1 Pathway.Cardiovascular drugs and therapy · 2026Article
- Time-Restricted Feeding Delays Cardiovascular Aging by Increasing Acetic Acid Through Remodeling Gut Microbiota.Aging cell · 2026Article
- ZBED6 deficiency drives pathological cardiac hypertrophy through MEOX1-ERK1/2-dependent autophagy dysfunction.PLoS genetics · 2026Article
- Age-dependent effects of aerobic training on cardiac expression of Akt1, mTOR, and CITED4 in immature, young-adult, and middle-aged rat myocardium.European journal of applied physiology · 2026Article
- SYVN1-mediated succinate accumulation exacerbates heart failure.Science China. Life sciences · 2026Article
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- An integrated overview of acute heart failure: a narrative review of pathophysiological mechanisms and contributing factors.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026Review
- Extracellular signal-regulated kinase 3 forms a nuclear complex with Aly/REF export factor and the splicing factor proline and glutamine rich to exacerbate pathological cardiac remodeling due to pressure overload.Molecular biomedicine · 2026Article
- Integration of multiple perspectives to understand the left ventricular pressure-volume relationship.Communications medicine · 2026Review
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- Synthetic Fructoborate Administration: Effects on Cardiac Remodeling and Extracardiac Responses in Isoproterenol-Induced Cardiac Hypertrophy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Leveraging neural network models for drug repurposing: a case study on cardiac hypertrophy.Scientific reports · 2026Article
- Vasohibin 1 acts as a key regulator of arrhythmogenesis in pressure-overload-induced cardiac hypertrophy.Acta pharmacologica Sinica · 2026Article
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Dynamic cardiac hyperplasia and hypertrophy in Burmese pythons.American journal of physiology. Cell physiology · 2026Article
882 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. There are two types of hypertrophy: physiological and pathological. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure. Each form of hypertrophy is regulated by distinct cellular signalling pathways. In the past decade, a growing number of studies have suggested that previously unrecognized mechanisms, including cellular metabolism, proliferation, non-coding RNAs, immune responses, translational regulation, and epigenetic modifications, positively or negatively regulate cardiac hypertrophy. In this Review, we summarize the underlying molecular mechanisms of physiological and pathological hypertrophy, with a particular emphasis on the role of metabolic remodelling in both forms of cardiac hypertrophy, and we discuss how the current knowledge on cardiac hypertrophy can be applied to develop novel therapeutic strategies to prevent or reverse pathological hypertrophy.
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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.