Figure 2.

Galectin-1 effects in different organs (arrow up or down) reported in pre-clinical studies (animal models and human cells), which should be confirmed in human tissues and clinical studies. Galectin-1 has been shown to improve tissue recovery after a cerebral stroke [101,102]. Galectin-1 also increases neovascularization and unwanted vascular proliferation in diabetic retinopathy [42,103,104]. In the pancreas, galectin-1 has been shown to stimulate insulin secretion in female mice, and circulating galectin-1 is also positively associated with serum insulin in studies in humans [47,64,80]. Studies have linked galectin-1 to adipogenesis, and it has been proposed that galectin-1 could directly affect pparg expression [23,72]. Galectin-1 has also been shown to reduce thermogenesis in mice [23,82]. In the liver, inhibition of galectin-1 results in increased fibrosis and increased severity of hepatitis [105], and galectin-1 reduces inflammation in the heart after ischaemia [106,107]. Galectin-1 also appears to facilitate skeletal muscle regeneration in muscle degenerative conditions, as well as in muscle damage [108]. In the kidney, results have been conflicting, as a Mendelian randomization study in humans and an intervention study in mice have demonstrated kidney protective effects of galectin-1 [43,47]. Conversely, circulating galectin-1 has been associated with a lower kidney function in cross-sectional and longitudinal studies [47,48], and in vitro studies have demonstrated contradicting associations with different fibrotic markers [95,96,109].