World Journal of Cardiovascular Diseases, Journal Year: 2024, Volume and Issue: 14(12), P. 739 - 756
Published: Jan. 1, 2024
Language: Английский
Journal of Cardiac Failure, Journal Year: 2024, Volume and Issue: unknown
Published: Sept. 1, 2024
Language: Английский
Citations
32
Journal of Cardiac Failure, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
During the last century characteristics of patients with heart failure (HF) and acute HF (AHF) have shifted from severe pump due to rheumatic, hypertensive ischemic disease older more obese multiple comorbidities. The pathophysiology AHF has in parallel that advanced, end-stage, caused by left ventricular dysfunction age, obesity comorbidity-related cardiovascular combined neurohormonal inflammatory dysregulation or "inflammaging". With advent blockers leading improved outcomes chronic HF, focus therapy also changed care directed at early symptom improvement therapies towards longer-term improvements quality life outcomes. Studies conducted 5 years suggest beneficial effects seen 4 pillars guideline-directed medical for mostly comprising blockade, can be extended when these are initiated rapidly uptitrated during admission after discharge. A recent pilot study (CORTAHF) suggested benefits treating markers activation anti-inflammatory therapies. Future studies should further examine whether blockade lead reversal disrupted underlying remission AHF.
Language: Английский
Citations
1
Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 101, P. 102542 - 102542
Published: Oct. 12, 2024
Language: Английский
Citations
4
World Journal of Cardiology, Journal Year: 2025, Volume and Issue: 17(1)
Published: Jan. 21, 2025
Heart failure (HF) is a complex syndrome characterized by the reduced capacity of heart to adequately fill or eject blood. Currently, HF remains leading cause morbidity and mortality worldwide, imposing substantial burden on global healthcare systems. Recent advancements have highlighted therapeutic potential mesenchymal stromal cells (MSCs) in managing HF. Notably, umbilical cord-derived MSCs (UC-MSCs) demonstrated superior clinical compared traditional bone marrow-derived MSCs; this evident their non-invasive collection process, higher proliferation efficacy, lower immunogenicity tumorigenicity, as substantiated preclinical studies. Although feasibility safety UC-MSCs been tested animal models, application treatment challenged issues such inaccurate targeted migration low survival rates UC-MSCs. Therefore, further research trials are imperative advance
Language: Английский
Citations
0
Journal of Cardiothoracic and Vascular Anesthesia, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0
SCRIPTA MEDICA, Journal Year: 2025, Volume and Issue: 56(1), P. 117 - 136
Published: Jan. 1, 2025
Extensive work over the past 6 decades in field of cardiovascular medicine has revealed that haemodynamic, hormonal, metabolic, cellular and molecular mechanisms heart failure are not only complex but also dependent upon type stage disease. Although various agents such as b-adrenoreceptor blockers, angiotensin converting enzyme inhibitors, II receptor antagonists vasodilators available for treatment failure, these interventions delay progression without reducing mortality morbidity. In this article, literature on pathophysiology due to myocardial infarction haemodynamic overload identify targets future drug development is reviewed. Particularly, objective was focus involving pathways generation oxidative stress, inflammation Ca2+-handling abnormalities. It evident elevated levels plasma vasoactive hormones growth factors well increased preload afterload play critical roles stimulating signal transduction occurrence ventricular wall cardiac remodelling subsequent dysfunction. These alterations associated with inflammation, endothelial dysfunction, metabolic defects, intracellular abnormalities, apoptosis, fibrosis changes extracellular matrix. view pathogenic abnormalities failing hearts, it suggested parameters may serve excellent therapy failure. addition, there occurs activation proteases phospholipases depression gene expression induction subcellular hearts thus affecting be considered exert beneficial effects There an urgent need develop some existing newer antioxidants sodium-glucose cotransporter-2 inhibitors RNA based therapies
Language: Английский
Citations
0
European Journal of Heart Failure, Journal Year: 2025, Volume and Issue: unknown
Published: April 9, 2025
Language: Английский
Citations
0
Nature Cardiovascular Research, Journal Year: 2024, Volume and Issue: 3(7), P. 819 - 840
Published: July 5, 2024
The molecular mechanisms of progressive right heart failure are incompletely understood. In this study, we systematically examined transcriptomic changes occurring over months in isolated cardiomyocytes or whole tissues from failing and left ventricles rat models pulmonary artery banding (PAB) aortic (AOB). Detailed bioinformatics analyses resulted the identification gene signature, protein transcription factor networks specific to compensated decompensated disease states. Proteomic RNA-FISH confirmed PAB-mediated regulation key genes revealed spatially heterogeneous mRNA expression heart. Intersection PAB-specific sets with transcriptome datasets human patients chronic thromboembolic hypertension (CTEPH) led more than 50 whose levels correlated severity disease, including multiple matrix-regulating secreted factors. These data define a conserved, differentially regulated genetic network associated rats humans.
Language: Английский
Citations
3
Angewandte Chemie International Edition, Journal Year: 2024, Volume and Issue: unknown
Published: Sept. 18, 2024
Ventricular arrhythmias (VAs) triggered by myocardial infarction (MI) are the leading cause of sudden cardiac mortality worldwide. Current therapeutic strategies for managing MI-induced VAs, such as left stellate ganglion resection and ablation, suboptimal, highlighting need to explore safer more effective intervention strategies. Herein, we rationally designed two supramolecular sonosensitizers RuA RuB, engineered through acceptor modification generate moderate reactive oxygen species (ROS) modulate VAs. Both RuB demonstrated high ultrasound (US)-activated ROS production efficiency, with singlet (
Language: Английский
Citations
3
Cells, Journal Year: 2024, Volume and Issue: 13(23), P. 2001 - 2001
Published: Dec. 4, 2024
Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among various regulatory systems that impact on these heterogeneous processes, angiotensin II (Ang II)-activated macrophages play pivotal role induction of subcellular defects adverse remodeling during progression heart failure. Ang stimulates via its AT1 receptor to release oxygen-free radicals, cytokines, chemokines, other mediators myocardium, upregulates expression integrin adhesion molecules both monocytes endothelial cells, leading monocyte-endothelial cell-cell interactions. The transendothelial migration monocyte-derived exerts biological effects proliferation fibroblasts, deposition extracellular matrix proteins, perivascular/interstitial development hypertension, hypertrophy Inhibition macrophage activation using antagonist or depletion from peripheral circulation has shown inhibitory II-induced vascular myocardial injury. purpose this review discuss current understanding maladaptive dysfunction, particularly focusing molecular signaling pathways involved macrophages-mediated In addition, challenges remained translating findings treatment patients are also addressed.
Language: Английский
Citations
3