[Show abstract][Hide abstract] ABSTRACT: The thrombospondins are a 5-member gene family that mediate cell-cell and cell-matrix interactions. The thrombospondins are either trimers or pentamers, and their functions depend on their abilities to interact with numerous extracellular ligands and cell surface receptors through the multiple domains that compose each subunit. Recent genetic studies have indicated associations of particular single nucleotide polymorphisms in 3 of the 5 thrombospondins with cardiovascular disease. This observation has stimulated efforts to understand how the thrombospondins influence cardiovascular pathology, to dissect how the individual polymorphisms alter the structure and function of the parent thrombospondin molecules, and to replicate the genetic data in different patient populations. This review seeks to summarize current information that has emerged on each of these fronts.
[Show abstract][Hide abstract] ABSTRACT: In addition to its major structural elements, extracellular matrix contains a number of factors that are important for orchestrating
developmental morphogenesis, maintaining tissue homeostasis in adults, and regenerating tissue following injury. Several proteins
that serve these functions share a complex modular structure that enables them to interact with specific components of the
matrix while engaging specific cell surface receptors through which they control cell behavior. These have been named matricellular
proteins. Matricellular proteins, including the thrombospondins, some thrombospondin-repeat superfamily members, tenascins,
SPARC, CCN proteins, and SIBLING proteins, are increasingly recognized to play important roles in inherited disorders, responses
to injury and stress, and the pathogenesis of several chronic diseases of aging. Improved understanding of the functions and
mechanisms of action of matricellular proteins is beginning to yield novel therapeutic strategies for prevention or treatment
of these diseases.
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