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Causes
Junctophilin (JPH)-2 is a critical mediator of t-tubule structure and function. In cardiac myocytes, mis localization or loss of JPH-2 protein results in pathological t-tubule remodelling, causing heart failure. Several studies have documented the role of microtubules in JPH-2-associated derangements, but the relationship between microtubules and JPH-2 has not been investigated in other heart failure models.
Previous studies suggested that t-tubule alterations were associated with microtubule-mediated mishandling of calcium in mdx cardiac myocytes. This study is the first to directly address this relationship and its role in heart failure. It found that t-tubule disruptions were associated with both the mis localization of JPH-2 and the reduction in JPH-2 protein.
The study also showed that in mdx hearts
The microtubules were depolymerized with the treatment of colchicine. This induced JPH-2 restoration and improved the organization of the t-tubule architecture. However, the amplitude of calcium transients was unchanged. Further studies are needed to determine the effects of normalizing JPH-2 through multiple mechanisms, including gene transfer, treatment with colchicine, and micro-RNA inhibition.
Overall, this study provides a molecular explanation for t-tubule dysfunction in Duchenne cardiomyopathy. It also suggests that JPH-2 plays a crucial role in t-tubule integrity. Furthermore, this study suggests that the abnormal calcium handling and the t-tubule derangements observed in mdx cardiac myocytes are related. These findings suggest that JPH-2 is a molecular mediator of t-tubule derangements and that correction of these alterations can prevent the development of heart failure.
Future studies are needed to better understand the role of microtubules and JPH-2 in heart failure. Additional studies are necessary to further explore the effects of JPH-2 overexpression, gene transfer, micro-RNA inhibition, and colchicine treatments on the development of heart failure. Moreover, future studies will need to identify the molecular mechanisms underlying t-tubule derangements in Duchenne cardiomyopathy. Moreover, a comprehensive review of the JPH gene family is needed to understand the biogenesis of JPH and its functional roles in excitable cells.
Junctophilins are structural proteins that form highly organized subcellular junctions, connecting plasma membrane to intracellular organelles. They play important signaling and tethering functions in all excitable cell types.
