Role of CaV1.2 in Tendon Formation
Tensile-bearing tendons are highly prone to acute injury and chronic degeneration from overuse, processes called tendinopathies. Therapeutic options for tendinopathies remain few due to limited knowledge about the basic biology underlying tendon development and postnatal tendon growth. Ca2+ signals have been implicated in tendon mechanotransduction, acting as second messengers to convert mechanical load to biochemical signals. However, Ca2+ signaling details in tendon and the source(s) of the increase in intracellular Ca2+ in tendon fibroblasts are largely unknown.
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Role of CaV1.2 in Heterotopic Bone (HO) Formation
HO is an ectopic and pathological bone formation in extraskeletal tissues, including skeletal muscle, fascia, tendons and ligaments and can be induced by traumatic injury or in patients with genetic disorders. HO causes pain and reduces range of motion that progresses to immobilization and devastates health and daily life. No treatment is currently available and the precise pathophysiology of HO remains unknown. Therefore, better understanding of the cellular and molecular mechanisms that underlie the dysregulated mesenchymal progenitor cell commitment and of the signaling pathways involved in the disease processes is in need to identify therapeutic strategies that can prevent HO initiation and/or progression.
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