ArticleEndocrine, metabolic & immune disorders drug targets2026
IGFBP2 Knockdown Ameliorates Diabetic Gastroparesis by Inhibiting VDAC1-Dependent Mitophagy in Interstitial Cells of Cajal
Article in Endocrine, metabolic & immune disorders drug targets, 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
INTRODUCTION/
objectiveAlthough insulin-like growth factor binding protein 2 (IGFBP2) is significantly upregulated in diabetic gastroparesis (DGP) and may regulate interstitial cells of Cajal (ICC) mitophagy through its interaction with voltage-dependent anion channel 1 (VDAC1), the precise mechanism of action remains unclear. This study aims to investigate the role and mechanism of IGFBP2 in the pathogenesis of DGP, with a specific focus on its impact on mitochondrial quality control in ICCs.
methodsAn in vivo DGP model was established. IGFBP2 expression was knocked down to assess its effects on systemic metabolism (blood glucose, HbA1c), gastric motor function (gastric emptying, motility, blood flow), and ICC integrity. In vitro, cell viability, apoptosis, mitochondrial membrane potential (MMP), and key proteins in the PINK1/Parkin mitophagy pathway were analyzed using CCK-8, flow cytometry, fluorescent probes, and Western blot.
resultsIGFBP2 knockdown significantly ameliorated hyperglycemia, promoted gastric emptying, enhanced contractile activity, and improved gastric perfusion. Mechanistically, it enhanced ICC survival, suppressed apoptosis, reduced mitochondrial oxidative stress, and stabilized MMP. Crucially, these benefits were mediated by the downregulation of VDAC1 and subsequent inhibition of PINK1/Parkin-dependent mitophagy. DISCUSSION: These findings indicate that IGFBP2 drives mitochondrial dysfunction and ICC loss via a VDAC1-dependent mitophagy pathway, revealing a previously underrecognized mechanism in DGP. The observed functional recovery and cytoprotection following IGFBP2 knockdown suggest that targeting this pathway may offer a potential therapeutic strategy for DGP.
conclusionIGFBP2 acts as a potential upstream regulator that drives mitochondrial dysfunction and ICC loss in DGP via a VDAC1-mitophagy axis. These findings unveil IGFBP2 as a promising therapeutic target for intervening in the progression of DGP.
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