Acute kidney injury (AKI) is a complex clinical condition characterized by rapid loss of renal function and high mortality rates [1]. Left untreated, AKI will lead to chronic kidney disease, which is almost irreversible. AKI is well documented to be caused by cellular processes such as acute tubular necrosis, obstruction, cytokine release, oxidative stress, inflammation, and apoptosis. however, the underlying molecular mechanisms remain incompletely understood [2]. At present, besides supportive care in the form of dialysis, the treatment of AKI in clinical practice is limited by the lack of effective drugs.

Icariin is a primary active ingredient in Epimedium brevicornu Maxim, a traditional Chinese medicine with a wide range of pharmacological functions. Research has proved that icariin can mitigate cisplatin-induced AKI, mainly by downregulating the levels of the proinflammatory factor TNFA as well as inhibiting NF-κB and apoptosis-related proteins [3]. Icariin can also reduce the mortality rate associated with sepsis-induced AKI by reducing oxidative damage, the inflammatory response, and proapoptotic signaling [4]. Based on the findings of these studies, icariin exhibits promise as a viable pharmaceutical agent for the clinical management of AKI. However, whether icariin can ameliorate FA-induced AKI is unknown.

In this research, we demonstrated that icariin has a significant therapeutic effect on FA-induced AKI. This is the first study to investigate the molecular mechanisms underlying FA-induced AKI and the therapeutic mechanism of icariin using proteomics.