AI Article Synopsis
- Ventricular remodeling in right heart failure (RHF) is a complex process involving neuro-hormonal activation, oxidative stress, cytokine expression, cardiomyocyte apoptosis, and changes in the extracellular matrix.
- This remodeling leads to myocardial hypertrophy and fibrosis, which negatively impacts heart function.
- Understanding these mechanisms is crucial for developing better treatments to enhance survival and quality of life for RHF patients, though research in this area remains limited.
Article Abstract
Ventricular remodeling in right heart failure is a complex pathological process involving interactions between multiple mechanisms. Overactivation of the neuro-hormonal pathways, activation of the oxidative stress response, expression of cytokines, apoptosis of cardiomyocytes, and alterations of the extracellular matrix (ECM) are among the major mechanisms involved in the development of ventricular remodeling in right heart failure. These mechanisms are involved in ventricular remodeling, such as myocardial hypertrophy and fibrosis, leading to the deterioration of myocardial systolic and diastolic function. A deeper understanding of these mechanisms can help develop more effective therapeutic strategies in patients with right heart failure (RHF) to improve patient survival and quality of life. Despite the importance of ventricular remodeling in RHF, there are a limited number of studies in this field. This article explores in-depth historical and current information about the specific mechanisms in ventricular remodeling in RHF, providing a theoretical rationale for recognizing its importance in health and disease.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683703 | PMC |
| http://dx.doi.org/10.31083/j.rcm2512426 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Treating myocardial infarction via a nano-ultrasonic contrast agent-mediated high-efficiency drug delivery system targeting macrophages.
Sci Adv
January 2025
Department of Cardiac Surgery, Peking University Third Hospital, Beijing 100191, China.
Following myocardial infarction (MI), the accumulation of CD86-positive macrophages in the ischemic injury zone leads to secondary myocardial damage. Precise pharmacological intervention targeting this process remains challenging. This study engineered a nanotherapeutic delivery system with CD86-positive macrophage-specific targeting and ultrasound-responsive release capabilities.
View Article and Find Full Text PDFPulmonary artery (PA) flow analysis is crucial for understanding the progression of pulmonary hypertension (PH). We hypothesized that PA flow characteristics vary according to PH etiology. In this study, we used 4D flow cardiovascular magnetic resonance imaging (CMR) to compare PA flow velocity and wall shear stress (WSS) between patients with pulmonary arterial hypertension (PAH) and those with heart failure with preserved ejection fraction and pulmonary hypertension (PH-HFpEF).
View Article and Find Full Text PDFSubclinical target organ damage in a sample of children and adolescents with solitary functioning kidney. A pilot study.
J Hypertens
February 2025
Department of Medicine.
Background: Patients with solitary functioning kidney appear to be exposed to an increased cardiovascular risk. This study aimed to evaluate the impact of peripheral and central blood pressure on subclinical cardiovascular organ damage in a sample of children and adolescents with solitary functioning kidney.
Methods: Carotid ultrasonography was performed to measure the carotid intima-media thickness (cIMT) and the carotid distensibility coefficient.
Recombinant dsAAV9-mediated Endogenous Overexpression of Macrophage Migration Inhibitory Factor Alleviates Myocardial Ischemia-Reperfusion Injury via Activating AMPK and ERK1/2 Signaling Pathways.
Cardiovasc Drugs Ther
January 2025
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Clinical Medical Research Institute, Xinjiang Medical University, No. 137 Liyushan South Road, Urumqi, 830054, China.
Purpose: To investigate the protective effect and mechanism of enhanced expression of endogenous macrophage migration inhibitory factor (MIF) on cardiac ischemia-reperfusion (I/R) injury.
Methods: A recombinant double-stranded adeno-associated virus serotype 9 with MIF or green fluorescent protein (GFP) genes (dsAAV9-MIF/GFP) was transduced into mice and neonatal rat ventricular myocytes (NRVMs). The models of cardiac 60 min ischemia and 24 h reperfusion and 12 h hypoxia/12 h reoxygenation (H/R) were established in mice and NRVMs, respectively.
Mechanical regulation of macrophage metabolism by allograft inflammatory factor 1 leads to adverse remodeling after cardiac injury.
Nat Cardiovasc Res
January 2025
Department of Pathology, Northwestern University, Chicago, IL, USA.
Myocardial infarction (MI) mobilizes macrophages, the central protagonists of tissue repair in the infarcted heart. Although necessary for repair, macrophages also contribute to adverse remodeling and progression to heart failure. In this context, specific targeting of inflammatory macrophage activation may attenuate maladaptive responses and enhance cardiac repair.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!