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| http://dx.doi.org/10.2147/DDDT.S405817 | DOI Listing |
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Dichloroacetate: A metabolic game-changer in alleviating macrophage inflammation and enhancing recovery after myocardial infarction.
Cell Signal
January 2025
Department of Cardiovascular Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China; Future Medical laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. Electronic address:
Background: Dichloroacetate (DCA) has shown potential in modulating cellular metabolism and inflammation, particularly in cardiac conditions. This study investigates DCA's protective effects in a mouse model of myocardial infarction (MI), focusing on its ability to enhance cardiac function, reduce inflammation, and shift macrophage polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype.
Methods: An acute MI model was created using left anterior descending coronary artery ligation.
Minimal extra-cardiac atherosclerosis present in young people with sudden cardiac death due to coronary artery disease.
Eur J Prev Cardiol
January 2025
St Vincent's Institute of Medical Research, 9 Princes St Fitzroy VIC 3065 Australia.
Aim: To define the association between severe coronary artery disease and widespread atherosclerosis in younger individuals.
Methods: Individuals aged 1-50 years with sudden cardiac death (SCD) from 2019-23, autopsy-proven to be due to coronary artery disease, were identified using the state-wide EndUCD registry. Presence of extra-coronary atherosclerosis greater than modified American Heart Association class III was assessed in 5 arterial beds (intra-cerebral vessels, aorta, carotid, renal and femoral arteries).
ERK1/2 Inhibition Alleviates Diabetic Cardiomyopathy by Suppressing Fatty Acid Metabolism.
Front Biosci (Landmark Ed)
January 2025
Department of Biomedical Sciences, Grand Valley State University, Allendale, MI 49401, USA.
Background: Diabetes mellitus is associated with morphological and functional impairment of the heart primarily due to lipid toxicity caused by increased fatty acid metabolism. Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) have been implicated in the metabolism of fatty acids in the liver and skeletal muscles. However, their role in the heart in diabetes remains unclear.
View Article and Find Full Text PDFJoint Group and Multi Institutional Position Opinion: Cirrhotic Cardiomyopathy-From Fundamentals to Applied Tactics.
Medicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
View Article and Find Full Text PDFImmunological Regulation of Fibrosis During Heart Failure: It Takes Two to Tango.
Biomolecules
January 2025
Heart and Vascular Institute, Pennsylvania State University Hershey Medical Center, Hershey, PA 17033, USA.
Immuno-fibrotic networks and their protein mediators, such as cytokines and chemokines, have increasingly been appreciated for their critical role in cardiac healing and fibrosis during cardiomyopathy. Immune activation, trafficking, and extravasation are tightly regulated to ensure a targeted and effective response against non-self antigens/pathogens while preserving tolerance towards self-antigens and coordinate fibrotic responses for efficient scar formation, a distinction that is severely compromised during chronic diseases. It is clear that immune cells are not only the critical regulators of post-infarct healing and scarring but are also the key players in regulating fibroblast activation during left-ventricular (LV) remodeling.
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