Itga11, encoding integrin α11 subunit which heterodimerizes with integrin β1 subunit to form integrin α11β1, is involved in multiple biological processes. It participates in cell-matrix interactions and is associated with pathways like Pi3k/Akt signaling pathway [3,4]. Itga11 is crucial for processes such as osteogenic differentiation, immune-related regulation, and has potential implications in various diseases [2,3]. Gene-knockout mouse models are valuable tools to study its functions.

In a PDGFRα+ITGA11+ CAFs-specific deficient mouse model, PDGFRα+ITGA11+ CAFs were found to promote lymphovascular invasion and lymphatic metastasis in early-stage bladder cancer, through the ITGA11-SELE interplay to activate the SRC-p-VEGFR3-MAPK pathway [1]. In Itga11 gene-deleted (Itga11-/-) mice, the integrin α11 subunit was shown to contribute to the clinical, histopathological, and molecular features of murine psoriasiform dermatitis, with reduced fibroblasts and inflammatory cells in skin samples upon disease induction [4]. In the preclinical MMTV-PyMT mouse model, integrin α11-deficiency led to a drastic reduction of breast cancer progression and metastasis, as integrin α11 promotes CAF invasion and CAF-induced tumor cell invasion via PDGFRβ/JNK signalling axis [5]. Integrin α11 deficiency in limb mesenchymal progenitors or chondrocytes in mice reduced growth plate chondrocyte proliferation and bone elongation [6].

In conclusion, Itga11 is essential for processes like osteogenic differentiation, skin inflammation regulation, cancer metastasis, and bone elongation. Gene-knockout mouse models have been instrumental in revealing its role in diseases such as early-stage bladder cancer, breast cancer, and psoriasiform dermatitis, providing insights into potential therapeutic targets.