<b>FcRn </b><b>upregulation</b><b> Exacerbates Podocyte Injury via Insulin Resistance-Induced Autophagy Disorder in Diabetic kidney disease</b>

<jats:p>&lt;p dir="ltr"&gt;Diabetic kidney disease (DKD) remains the leading cause of end-stage renal disease (ESRD) worldwide despite therapeutic advances. Podocyte injury constitutes a critical pathogenic process in DKD. This study elucidated the role of the neonatal Fc receptor (FcRn) in DKD-associated podocyte injury. In DKD, glomerular FcRn expression was markedly elevated and inversely correlated with podocin levels. In diabetic mice, podocyte-specific FcRn deficiency significantly ameliorated insulin resistance and mitigated podocyte damage. Mechanistically, FcRn &lt;a href="" target="_blank"&gt;upregulation&lt;/a&gt; in diabetic podocytes exacerbated insulin resistance, suppressed AKT/mTOR signaling, and impaired autophagy, thereby promoting podocyte injury. &lt;a href="" target="_blank"&gt;These findings identify FcRn as a pivotal contributor to podocyte injury in DKD and suggest that FcRn targeting represents a promising therapeutic strategy.&lt;/a&gt;&lt;/p&gt;</jats:p>