ArticleApplied biochemistry and biotechnology2026
Circ_0039857: A Key Player in Combating Immune Disorders and Ferroptosis in High-Glucose-induced HK-2 Cells and Diabetic Kidney Disease Mice.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetic kidney disease (DKD) is a microvascular complication associated with diabetes. Circ_0039857 has been shown to exert regulatory functions in various human diseases. This research aimed to elucidate the role and mechanism of circ_0039857 in DKD. Our findings revealed that both circ_0039857 and miR-4739 expressions were decreased in DKD, while PON1 levels were elevated. Functionally, circ_0039857 overexpression repressed immune disorders and ferroptosis in HG-induced HK-2 cells. Mechanistically, circ_000888 was bound to miR-4739, and miR-4739 was bound to PON1. Meanwhile, the effects of circ_0039857 overexpression on immune disorder and ferroptosis in HG-induced HK-2 cells were abolished after miR-4739 mimic or si-PON1 co-transfection, revealing the key regulatory function of circ_0039857/miR-4739/PON1 axis in DKD. Furthermore, circ_0039857 repressed DKD progression in vivo, mainly by reducing the proliferation of renal mesangial cells and renal collagen deposition in DKD mice. Also, circ_0039857 reduced immune disorders and ferroptosis in in vivo model of DKD. In summary, circ_0039857 overexpression inhibited immune disorders and ferroptosis by targeting miR-4739/PON1, thus alleviating DKD.
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