In conclusion, our study highlights the pivotal role of Gal-3 in AKI by initiating a systemic inflammatory response, potentially triggering a systemic cascade that promotes CD146-mediated endothelial interaction, cytokine secretion, and immune cell infiltration in renal tissue, further contributing to organ fibrosis and subclinical dysfunction (Figure S10). The gene discussed is LGALS3; the disease is acute kidney injury.