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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
We previously identified vaspin as a gene upregulated in visceral adipose tissue of OLETF rats, animal model of obesity and type 2 diabetes (PNAS, 2005), and demonstrated its protective roles against obesity, insulin resistance, fatty liver, and atherosclerosis (Diabetes, 2012) (Circ Res, 2013). Circulating vaspin is filtered by the glomerulus and taken up by proximal tubular cells, where it mitigates obesity-induced endoplasmic reticulum stress, defective autophagy, lysosomal membrane permeabilization, and NLRP3 inflammasome activation, thereby protecting tubular cells (Commun Biol, 2021). However, the effects of vaspin on mitochondria remain unclear. This study aimed to elucidate the role of vaspin in mitochondrial dynamics in diabetic kidney disease.
Diabetes was induced by streptozotocin (STZ) in Vaspin knockout (Vaspin-/-), wild-type, and vaspin transgenic (Tg) mice. In vitro, HK-2 cells were exposed to diabetic stressors with or without recombinant vaspin. Changes in molecules related to mitochondrial dynamics were analyzed, and mitochondrial morphology was assessed using Mitotracker staining. Molecules interacting with vaspin were identified, and their functions were further investigated.
STZ-induced diabetic Vaspin-/- mice developed onion layer-like structure of mitochondria in tubular cells. It confirmed by 3D electron microscopy that fragmented mitochondria were concentrically surrounded by flattened, disc-like mitochondria forming multilayered cup-shaped structures. Vaspin-/- mice exhibited tubular thinning, luminal dilatation, interstitial fibrosis, and increased NOX4-positive tubular area, whereas these changes were ameliorated in Vaspin Tg mice. In HK-2 cells, H2O2 stimulation reduced Mfn1 and Mfn2, increased p62, and induced mitochondrial fragmentation; these alterations were attenuated by vaspin. Similar protective effects were observed upon carbonyl cyanide m-chlorophenyl hydrazone (CCCP), uncoupler, -induced mitophagy. The effect of vaspin on mitochondrial dynamics was linked to HSPA1L, identified as one of vaspin-interacting protein. Overexpression of HSPA1L increased Mfn1/2 levels, counteracting their degradation by the E3 ubiquitin ligase Autocrine Motility Factor Receptor (AMFR). H2O2 decreased HSPA1L, while CCCP increased AMFR with concomitant Mfn1/2 reduction; both were alleviated by vaspin. Next, HSPA1L has been reported to form a complex with Parkin to promote mitophagy. We identified a novel complex partner of HSPA1L that modulates mitochondrial dynamics in the diabetic kidney.
Vaspin ameliorates diabetic tubulointerstitial injury by regulating mitochondrial dynamics through HSPA1L. These findings reveal a novel mechanism linking vaspin to mitochondrial homeostasis and suggest therapeutic potential for targeting vaspin–HSPA1L signaling in diabetic kidney disease.
