The cardiac sodium current underlies excitability in heart, and inherited abnormalities of the proteins regulating and conducting this current cause inherited arrhythmia syndromes. This review focuses on inherited mutations in non-pore forming proteins of sodium channel complexes that cause cardiac arrhythmia, and the deduced mechanisms by which they affect function and dysfunction of the cardiac sodium current. Defining the structure and function of these complexes and how they are regulated will contribute to understanding the possible roles for this complex in normal and abnormal physiology and homeostasis. This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes".
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http://dx.doi.org/10.1016/j.yjmcc.2013.03.017 | DOI Listing |
J Chem Ecol
January 2025
Department of Nematology, University of California Riverside, Riverside, CA, USA.
Plants produce defensive toxins to deter herbivores. In response, some specialized herbivores evolved resistance and even the capacity to sequester toxins, affecting interactions at higher trophic levels. Here, we test the hypothesis that potential natural enemies of specialized herbivores are differentially affected by plant toxins depending on their level of adaptation to the plant-herbivore system.
View Article and Find Full Text PDFEur J Clin Invest
January 2025
Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Background: Transthyretin amyloid cardiomyopathy (ATTR-CM) commonly leads to heart failure but has traditionally been an exclusion criterion in randomized clinical trials (RCTs) of sodium-glucose cotransporter 2 inhibitors (SGLT2i); therefore, the effects of these drugs in this population remain undocumented. In light of recent studies, this meta-analysis aimed to investigate the effect of SGLT2i on the prognosis of patients with ATTR-CM.
Methods: A comprehensive search of Medline, Scopus, and the Cochrane Library was conducted up to November 17, 2024.
Am J Prev Cardiol
March 2025
Ahmanson-UCLA Cardiomyopathy Center, Division of Cardiology, University of California Los Angeles, Los Angeles, CA, USA.
Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have shown benefits in improving cardiovascular (CV) outcomes in patients with heart failure (HF) and may mitigate symptom progression in myocardial infarction (MI). However, their effectiveness in patients with type 2 diabetes and MI undergoing percutaneous coronary intervention (PCI) is unclear.
Methods: To identify eligible studies, a comprehensive search of electronic databases, PubMed, Cochrane Library, Scopus and Embase, was conducted from inception until May 2024.
Kidney Med
February 2025
Department of Internal Medicine, Research Methodology and Biostatistics Core, Office of Research, Morsani College of Medicine, University of South Florida Health, Tampa, FL.
Rationale & Objective: There are likely over 42 million patients with hypertension taking thiazides in the United States and many more worldwide. Hyponatremia is a common complication of thiazide therapy. It is not currently known if thiazide-associated hyponatremia is also associated with increased mortality.
View Article and Find Full Text PDFWorld J Cardiol
January 2025
Department of Cardiology, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan 030012, Shanxi Province, China.
This article discusses the study by Grubić Rotkvić on the mechanisms of action of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in patients with type 2 diabetes mellitus (T2DM) and heart failure (HF). T2DM and HF are highly comorbid, with a significantly increased prevalence of HF in patients with T2DM. SGLT2i exhibit potential in reducing hospitalization rates for HF and cardiovascular mortality through multiple mechanisms, including improving blood glucose control, promoting urinary sodium excretion, reducing sympathetic nervous system activity, lowering both preload and afterload on the heart, alleviating inflammation and oxidative stress, enhancing endothelial function, improving myocardial energy metabolism, and stabilizing cardiac ion homeostasis.
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