ReviewItalian journal of pediatrics2012
Molecular pathogenesis of myocardial remodeling and new potential therapeutic targets in chronic heart failure.
Review in Italian journal of pediatrics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Chrysin alleviates pressure overload-induced myocardial remodeling through regulating the PI3K/AKT/NRF2 pathway-mediated oxidative stress response.Animal models and experimental medicine · 2026Article
- Article
- Correlations of serum histone deacetylase 3 and thrombospondin-1 levels with cardiac function grades, ventricular remodeling, and prognosis in patients with chronic heart failure.Journal of cardiothoracic surgery · 2025Article
- Network pharmacology combined with experimental analysis to explore the mechanism of the XinShuaiNing formula on heart failure.3 Biotech · 2025Article
- Application value of myocardial work technology by non-invasive echocardiography in evaluating left ventricular function in patients with chronic heart failure.Quantitative imaging in medicine and surgery · 2022Article
- CD133+Exosome Treatment Improves Cardiac Function after Stroke in Type 2 Diabetic Mice.Translational stroke research · 2021Article
- Inflammatory responses mediate brain-heart interaction after ischemic stroke in adult mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Maternal exercise intervention in obese pregnancy improves the cardiovascular health of the adult male offspring.Molecular metabolism · 2018Article
- Promise of adeno-associated virus as a gene therapy vector for cardiovascular diseases.Heart failure reviews · 2017Review
- Wnt5a is elevated in heart failure and affects cardiac fibroblast function.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Cardioprotection against Heart Failure by Shenfu Injection via TGF-Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Tanshinone IIA Inhibits β-Catenin Nuclear Translocation and IGF-2R Activation via Estrogen Receptors to Suppress Angiotensin II-Induced H9c2 Cardiomyoblast Cell Apoptosis.International journal of medical sciences · 2017Article
- Left Ventricular Remodelling: A Problem in Search of Solutions.European cardiology · 2016Review
- Effect of Phosphatase and Tensin Homologue on Chromosome 10 on Angiotensin II-Mediated Proliferation, Collagen Synthesis, and Akt/P27 Signaling in Neonatal Rat Cardiac Fibroblasts.BioMed research international · 2016Article
- Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts.Molecular and cellular biochemistry · 2015Article
- Maternal diet-induced obesity programs cardiovascular dysfunction in adult male mouse offspring independent of current body weight.Endocrinology · 2014Article
- Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure.International journal of molecular medicine · 2014Article
- Exercise training reduces cardiac dysfunction and remodeling in ovariectomized rats submitted to myocardial infarction.PloS one · 2014Article
- AAV-mediated gene therapy for heart failure: enhancing contractility and calcium handling.F1000prime reports · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that the natural history of chronic heart failure (CHF),regardless of age and aetiology,is characterized by progressive cardiac dysfunction refractory to conventional cardiokinetic, diuretic and peripheral vasodilator therapy. Several previous studies, both in animals and humans, showed that the key pathogenetic element of CHF negative clinical evolution is constituted by myocardial remodeling. This is a complex pathologic process of ultrastructural rearrangement of the heart induced by various neuro-humoral factors released by cardiac fibrocells in response to biomechanical stress connected to chronic haemodynamic overload. Typical features of myocardial remodeling are represented by cardiomyocytes hypertrophy and apoptosis, extracellular matrix alterations, mesenchymal fibrotic and phlogistic processes and by cardiac gene expression modifications with fetal genetic program reactivation. In the last years, increasing knowledge of subtle molecular and cellular mechanisms involved in myocardial remodeling has led to the discovery of some new potential therapeutic targets capable of inducing its regression. In this paper our attention is focused on the possible use of antiapoptotic and antifibrotic agents, and on the fascinating perspectives offered by the development of myocardial gene therapy and, in particular, by myocardial regenerative therapy.
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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.