![]() ![]() ![]() However, TNC is re-expressed in the myocardium in response to a wide array of cardiac injuries. The heart of TNC knock-out (TNCKO) mice develop normally and show no sign of deficiency ( 16– 18). Nonetheless, TNC’s actions in the pathophysiology of cardiovascular disease in vivo remain uncertain. In different experimental models and tissues, TNC has been reported to mediate or inhibit cell adhesion ( 5– 9), induce or inhibit differentiation ( 10, 11), stimulate cell growth and survival ( 12, 13), and promote apoptosis ( 14, 15). Multiple functions have been attributed to TNC based upon its effects observed in cell culture and its distribution in tissues undergoing active restructuring. It is highly expressed during fetal development but its expression is downregulated in adult tissues. ![]() Tenascin-C (TNC) is a member of matricellular proteins with distinct spatial and temporal expression during development, tissue homeostasis, and disease ( 4). At the molecular level, these changes in cellular phenotype are accompanied by the re-expression of fetal gene program ( 3). At the cellular level, LVH is characterized by an increase in cell size, enhanced protein synthesis, and heightened organization of the sarcomere. LVH is a complex and multifactorial condition whose pathogenesis might include many different genetic and signaling pathways ( 2). Left ventricular hypertrophy (LVH) is a strong predictor of adverse cardiovascular outcomes and an important risk factor for sudden death and heart failure ( 1). ![]()
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