CRYAB, also known as α -Crystallin B, is a member of the small heat shock protein family. It functions as a chaperone, protecting interacting proteins from degradation. CRYAB is involved in multiple signaling pathways such as apoptosis, inflammation, oxidative stress, and ferroptosis, and is associated with various diseases including eye and heart diseases, and cancers like breast, lung, prostate, ovarian, and colorectal cancer [1,3].

In human bone marrow stem cells (BMSCs), knockdown of CRYAB decreased the expression of osteogenic markers and ALP activity, and promoted ferroptosis, indicating its role in suppressing ferroptosis and promoting osteogenic differentiation [2]. In colorectal cancer, knockdown of CRYAB induced ferroptosis, while its overexpression enhanced the stem-cell-like properties of cancer cells via the Wnt/β-catenin pathway [3,6]. In cardiomyocytes, overexpression of CRYAB protected against heat stress, myocardial ischemia-reperfusion (I/R) injury by reducing apoptosis and ferroptosis [4,5].

In conclusion, CRYAB plays essential roles in multiple biological processes such as osteogenic differentiation, cell survival under stress, and cancer progression. The findings from knockdown and over-expression experiments across different cell types highlight its significance in various disease areas, especially in bone, heart, and colorectal cancer-related conditions.