Integrin (osteogenic cell-specific subtypes)

Integrins are a family of transmembrane cell adhesion receptors that mediate the interaction between osteogenic cells—such as mesenchymal stem cells, osteoblasts, osteoclasts, and osteocytes—and the extracellular matrix (ECM)[4][7][1]. These receptors are crucial for transducing mechanical and biochemical signals that regulate bone cell adhesion, migration, proliferation, and especially differentiation into osteoblasts (osteogenic differentiation)[1][2][4]. Subtypes such as integrin α5β1 and α11β1 have been shown to specifically mediate osteogenic differentiation by interacting with ECM components (including fibronectin and collagen) and activating downstream signaling pathways (MAPK, PI3K, Wnt)[2][3][1]. The activity of these integrins is essential for bone formation, homeostasis, and repair, as well as for pathological processes such as osteoporosis, bone metastasis, and osteoarthritis[2][4][3]. Due to their central regulatory roles, integrins expressed by osteogenic cells are considered promising but complex therapeutic targets for skeletal diseases, with ongoing research targeting specific subunits or blocking integrin-ligand interactions[1][5]. Notes: - "Osteogenic cell integrins" is *not* a single defined molecular target; it is a collective term for the integrin family members expressed by osteogenic cells, primarily including but not limited to: α5β1, αVβ1, β1, α11β1, and others[1][2][3][4][5]. - For structured bioinformatics or drug discovery work, it is preferable to refer to and annotate individual integrin subunits (e.g., integrin α5β1 or integrin α11β1) rather than the generic "osteogenic cell integrins."[2][3][4] - No canonical abbreviation applies to the family as a whole; individual integrins (e.g., ITGA5, ITGB1) are used for specific subunits.

Other names

IntegrinsIntegrin receptorOsteogenic integrinsβ1 integrinsα5β1 integrinα11β1 integrinαVβ1 integrinCollagen-binding integrinsRGD-binding integrins

Modulation of cell-matrix adhesion; Inhibition or activation of integrin-ligand binding; Prevention of downstream signaling (MAPK, PI3K pathways); Allosteric antagonism (in general for integrin inhibitors).