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| http://dx.doi.org/10.1161/CIRCULATIONAHA.116.023648 | DOI Listing |
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Discovery of Titin and Its Role in Heart Function and Disease.
Circ Res
January 2025
Department of Integrative Pathophysiology, Medical Faculty Mannheim, DZHK Partnersite Mannheim-Heidelberg, University of Heidelberg, Germany (S.L.).
This review examines the giant elastic protein titin and its critical roles in heart function, both in health and disease, as discovered since its identification nearly 50 years ago. Encoded by the TTN (titin gene), titin has emerged as a major disease locus for cardiac disorders. Functionally, titin acts as a third myofilament type, connecting sarcomeric Z-disks and M-bands, and regulating myocardial passive stiffness and stretch sensing.
View Article and Find Full Text PDFThe heart adapts to cardiac demand through a variety of mechanisms. Some of these adaptations include chemical modifications of myofilament proteins responsible for cell contraction. Interestingly, many of these chemical modifications, such as phosphorylation, are found in unstructured, or intrinsically disordered, regions of proteins.
View Article and Find Full Text PDFTitin As the Culprit Behind Dilated Cardiomyopathy: A Case Series of Three Cases and a Comprehensive Literature Review.
Cureus
August 2024
Internal Medicine, CMH Multan Institute of Medical Sciences, Multan, PAK.
Nonischemic dilated cardiomyopathy (DCM) is a complex cardiovascular condition often characterized by genetic pathogenesis. Comprehensive genetic testing has become a crucial aspect of DCM diagnosis and management, offering insights into prognosis and the identification of at-risk individuals. We delve into distinct genetic pathways associated with DCM and their pathogenetic mechanisms, emphasizing the evolving significance of genetic markers, particularly in cases where arrhythmia risk is heightened.
View Article and Find Full Text PDFDifferential regulation of physicochemical properties and myofibrillar protein degradation of yak meat by interactions between reactive oxygen species and reactive nitrogen species during postmortem aging.
J Sci Food Agric
January 2025
College of Food Science and Engineering, Gansu Agricultural University, Lanzhou, China.
Background: This study aimed to explore how interactions between reactive oxygen species (ROS) and reactive nitrogen species (RNS) affect oxidative properties, nitrosative properties, and myofibrillar protein degradation during postmortem aging of yak meat.
Results: Yak longissimus dorsi was incubated with saline, ROS activator (HO)/inhibitor N-Acetyl-L-cysteine (NAC) and RNS activator S-Nitrosoglutathione (GSNO)/inhibitor L-NAME hydrochloride (L-NAME) combined treatments at 4 °C for 12, 24, 72, 120, and 168 h. The results indicated that regardless of whether RNS was activated or inhibited, activated ROS played a dominant role in myofibrillar protein degradation by oxidative modification to increase carbonyl content, disulfide bonds, surface hydrophobicity, and dimerized tyrosine while decreasing sulfhydryl content, thereby degrading nebulin, titin, troponin-t and desmin.
Modeling cardiomyocyte signaling and metabolism predicts genotype-to-phenotype mechanisms in hypertrophic cardiomyopathy.
Comput Biol Med
June 2024
Department of Mechanical and Aerospace Engineering, Jacobs School of Engineering, University of California San Diego, La Jolla CA 92093, United States of America. Electronic address:
Familial hypertrophic cardiomyopathy (HCM) is a significant precursor of heart failure and sudden cardiac death, primarily caused by mutations in sarcomeric and structural proteins. Despite the extensive research on the HCM genotype, the complex and context-specific nature of many signaling and metabolic pathways linking the HCM genotype to phenotype has hindered therapeutic advancements for patients. Here, we have developed a computational model of HCM encompassing cardiomyocyte signaling and metabolic networks and their associated interactions.
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