Potential Renoprotective Effects of Honokiol

Acute kidney injury (AKI) and chronic kidney disease (CKD), such as ischemia–reperfusion injury, renal sepsis, diabetic nephropathy, and renal fibrosis, remain major causes of morbidity and mortality around the world. Despite current therapeutic advances, progression to renal dysfunction and end-stage renal disease continues to be a major clinical concern. Honokiol, a low-molecular-weight natural product derived from Magnolia officinalis, has demonstrated numerous potential renoprotective effects on kidney disorders. The objective of this review was to discuss the latest findings on the protective effects of honokiol on a variety of models of kidney injury. These models include diabetic nephropathy, CKD by adenine administration, unilateral ureteral obstruction (UUO)-induced renal fibrosis, renal ischemia–reperfusion, and sepsis-induced acute kidney injury, as well as cyclosporin A, cadmium, and cisplatin renal toxicity. Numerous investigations on honokiol’s protective mechanisms focus on critical pathological processes such as mitochondrial dysfunction, reactive oxygen species generation, inflammatory signaling, and tissue remodeling. These studies indicate that honokiol demonstrates potential renoprotective effects by modulating multiple pathways, including SIRT3-mediated mitochondrial homeostasis, NLRP3 inflammasome activation, oxidative stress responses, Wnt/β-catenin signaling, and miR-218-5p/heme oxygenase-1 (HO-1) signaling. These mechanisms contribute to the preservation of mitochondrial homeostasis, reduction in renal inflammation, prevention of extracellular matrix accumulation, and improvement of kidney function in various experimental models. Our review ends with suggestions for future studies on the potential of honokiol as a possible therapeutic agent for the prevention and treatment of renal disorders.