KL and diabetic kidney disease: Pathological processes of diabetic nephropathy resemble kidney injury through cellular senescence [7], with a shortening of telomeres, DNA damage, epigenetic alterations, changes in protein patterns, mitophagy deficiencies, the downregulation of Klotho expression, inflammation, the activation of profibrotic Wnt/β-catenin signaling, and the accumulation of uremic toxins (e.g., indoxyl sulfate) that further reduce renal Klotho expression and intensify fibrosis [8,9,10,11,12].