Over recent years, preclinical and clinical evidence has implicated myocardial inflammation (M-Infl) in the pathophysiology and phenotypes of traditionally genetic cardiomyopathies. M-Infl resembling myocarditis on imaging and histology occurs frequently as a clinical manifestation of classically genetic cardiac diseases, including dilated and arrhythmogenic cardiomyopathy. The emerging role of M-Infl in disease pathophysiology is leading to the identification of druggable targets for molecular treatment of the inflammatory process and a new paradigm in the field of cardiomyopathies. Cardiomyopathies constitute a leading cause of heart failure and arrhythmic sudden death in the young population. The aim of this review is to present, from bedside to bench, the current state of the art about the genetic basis of M-Infl in nonischemic cardiomyopathies of the dilated and arrhythmogenic spectrum in order to prompt future research towards the identification of novel mechanisms and treatment targets, with the ultimate goal of lowering disease morbidity and mortality.
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http://dx.doi.org/10.3390/biom13040646 | DOI Listing |
PLoS One
January 2025
Department of Pediatrics, Quanzhou First Hospital, Quanzhou, Fujian Province, China.
Purpose: To systematically evaluate the efficacy and safety of creatine phosphate sodium in the treatment of viral myocarditis, and to provide guidance for its clinical treatment.
Methods: We conducted a search of The Cochrane Library, PubMed, EMbase, and Web of Science databases to retrieve randomized controlled trials (RCTs) on the use of creatine phosphate sodium (CPS) in the treatment of viral myocarditis. The search was conducted up to April 2024.
Immun Inflamm Dis
January 2025
Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Background: Sepsis is associated with myocardial injury and early mortality. The innate immune receptor Toll-like receptor 4 (TLR4) can recognize pathogen-associated-molecular-patterns (PAMPs) and damage-associated molecular patterns (DAMPs); the latter are released during tissue injury. We hypothesized that TLR4 inhibition reduces proinflammatory signaling and cytokine release in: (1) LPS or Escherichia coli-treated isolated mouse heart; (2) LPS-treated mouse primary adult cardiomyocytes; and (3) the isolated heart during ischemia-reperfusion.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Shanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Acute myocardial infarction (AMI) is associated with well-established metabolic risk factors, especially hyperlipidemia and obesity. Myocardial ischemia-reperfusion injury (mIRI) significantly offsets the therapeutic efficacy of revascularization. Previous studies indicated that disrupted lipid homeostasis can lead to lipid peroxidation damage and inflammation, yet the underlying mechanisms remain unclear.
View Article and Find Full Text PDFEgypt Heart J
January 2025
Intensivista Pediátrico, Fundación Clínica Infantil Club Noel, Cali, Colombia.
Background: The mitroaortic intervalvular fibrosa is an avascular structure near the left ventricular outflow tract, between the mitral and aortic valves. Mitroaortic intervalvular fibrosa complications, such as tamponade, hemopericardium, and abscesses, are rare and often diagnosed postmortem. On the other hand, the COVID-19 pandemic notably impacted pediatric patients with congenital heart diseases, who frequently presented cardiac complications including arrhythmias, elevated troponins, myocarditis, and heart failure.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Pharmacology, Central University of Punjab, Bathinda, Punjab, 151401, India.
Diabetic cardiomyopathy (DCM) represents a significant health burden, exacerbated by the global increase in type 2 diabetes mellitus (T2DM). This condition contributes substantially to the morbidity and mortality associated with diabetes, primarily through myocardial dysfunction independent of coronary artery disease. Current treatment strategies focus on managing symptoms rather than targeting the underlying pathophysiological mechanisms, highlighting a critical need for specific therapeutic interventions.
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