Table 1.
Attempts to target αV integrin function as a therapeutic strategy to treat TGF-β–associated disorders
| Integrin | Disorder | Experimental findings |
|---|---|---|
| αVβ3 | 1. Atherosclerosis | 1. Blockade of αVβ3 reduced neointima formation by reducing TGF-β activity [113] |
| αVβ5 | 2. Rheumatoid arthritis | 2. Integrin αVβ3 as a target for the treatment of rheumatoid arthritis and related rheumatic diseases [114] |
| 3. Systemic sclerosis | 3. Increased expression of integrin αVβ5 contributes to the establishment of autocrine TGF-β signalling in scleroderma fibroblasts [115] | |
| αVβ6 | 1. Inflammation | 1. αVβ6 protects against inflammatory periodontal disease through activation of TGF-β [98] |
| 2. Carcinoma | 2. Blockade of integrin αVβ6 inhibits tumour progression in vivo by a TGF-β regulated mechanism [70] | |
| 3. Fibrosis | 3. Inhibitors of αVβ6 integrin or TGF-β down-regulate fibrosis following acute or ongoing pulmonary, biliary injury, renal injury [68, 69] | |
| 4. Cataracts | 4. αVβ6 was hypothesized to be the main activator of TGF-β1 in the lens capsule and represents a possible target for the prevention of posterior capsular opacification [99] | |
| αVβ8 | 1. Immune dysfunction | 1. αVβ8-mediated TGF-β activation by dendritic cells is essential to prevent inflammatory bowel disease and autoimmunity [103] |
| 2. COPD | 2. αVβ8 integrin-mediated TGF-β activation amplifies pathologic epithelial-mesenchymal in chronic obstructive pulmonary disease patients [116] | |
| 3. Brain haemorrhage | 3. αVβ8 acts as a central regulator of brain vessel homeostasis through its regulation of TGF-β activation [102] |