ReviewJournal of clinical medicine2019
Advanced Evolution of Pathogenesis Concepts in Cardiomyopathies.
Review in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Phosphoinositides in membrane remodeling during infections and cellular stresses.FEBS letters · 2026Review
- PIP3 antagonist as a molecular regulator in MSC-derived cardiomyocytes: Potential in vitro therapeutic implications for conotruncal heart defects.Journal, genetic engineering & biotechnology · 2026Article
- Combination of reverse shock index and simplified motor score as a strong discriminator of trauma outcomes.Annals of medicine · 2025Article
- Association Between Diurnal Temperature Range and Risk of Cardiomyopathy-Induced Hospitalisation in Henan, China: A Time-Series Study.Risk management and healthcare policy · 2025Article
- An hiPSC-CM approach for electrophysiological phenotyping of a patient-specific case of short-coupled TdP.Stem cell research & therapy · 2024Article
- The Emerging Role of Epigenetics in Therapeutic Targeting of Cardiomyopathies.International journal of molecular sciences · 2021Review
- Genetic Restrictive Cardiomyopathy: Causes and Consequences-An Integrative Approach.International journal of molecular sciences · 2021Review
- Clinical Insights Into Heritable Cardiomyopathies.Frontiers in genetics · 2021Review
- Effects of Individual and Coexisting Diabetes and Cardiomyopathy on Diastolic Function in Rats (Comparative medicine · 2020Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Phosphoinositide Signaling and Mechanotransduction in Cardiovascular Biology and Disease.Frontiers in cell and developmental biology · 2020Review
- Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis.Oxidative medicine and cellular longevity · 2020Review
- [Research progress on miR-21 in heart diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Cardiomyopathy is a group of heterogeneous cardiac diseases that impair systolic and diastolic function, and can induce chronic heart failure and sudden cardiac death. Cardiomyopathy is prevalent in the general population, with high morbidity and mortality rates, and contributes to nearly 20% of sudden cardiac deaths in younger individuals. Genetic mutations associated with cardiomyopathy play a key role in disease formation, especially the mutation of sarcomere encoding genes and ATP kinase genes, such as titin, lamin A/C, myosin heavy chain 7, and troponin T1. Pathogenesis of cardiomyopathy occurs by multiple complex steps involving several pathways, including the Ras-Raf-mitogen-activated protein kinase-extracellular signal-activated kinase pathway, G-protein signaling, mechanotransduction pathway, and protein kinase B/phosphoinositide 3-kinase signaling. Excess biomechanical stress induces apoptosis signaling in cardiomyocytes, leading to cell loss, which can induce myocardial fibrosis and remodeling. The clinical features and pathophysiology of cardiomyopathy are discussed. Although several basic and clinical studies have investigated the mechanism of cardiomyopathy, the detailed pathophysiology remains unclear. This review summarizes current concepts and focuses on the molecular mechanisms of cardiomyopathy, especially in the signaling from mutation to clinical phenotype, with the aim of informing the development of therapeutic interventions.
Indexed as
Identifiers
What Socratic 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 Socratic graph.