Multifaceted elucidation of aminoguanidine in protecting against diabetes-induced vascular endothelial injury
Year: 2026
Type: article
Abstract: Chronic hyperglycemia-driven protein glycation in diabetes is a key pathogenic factor in vascular endothelial injury. This study demonstrates the multifaceted protective profile of aminoguanidine (AMG) against diabetes-induced vascular injury. As a carbonyl scavenger, AMG effectively traps methylglyoxal (MGO), inhibiting advanced glycation end products (AGEs) formation while preserving endothelial glycocalyx integrity and permeability. Mechanistically, AMG suppresses NF-κB-mediated inflammation, upregulates the eNOS/NO pathway, and restores CD31 expression, collectively mitigating oxidative stress, apoptosis and impaired proliferation in human umbilical vein endothelial cells (HUVECs). Metabolomic profiling further reveals AMG's capacity to alleviate MGO-induced metabolic dysregulation by modulating critical pathways, including glutathione metabolism and the TCA cycle. In diabetic mice, AMG attenuates site-specific glycation adducts on plasma albumin and demonstrates significant therapeutic efficacy by improving endothelial-dependent vasodilation via the eNOS/NO pathway, reducing vascular fibrosis and basement membrane thickening, and suppressing NF-κB-driven inflammatory responses. These integrated findings establish AMG as a promising therapeutic candidate with multifaceted protective effects against diabetic vascular injury.
DOI: 10.3724/abbs.2026005
Authors: Huiru Tang, Yuhan Zhai, Gaojun Wang, Junfeng Shi, Yuxue Li, Zhipeng Wang, Yudong Guan, Kexin Zhang, Wenshuang Wang, Qinying Li, Xiaodong Sun, Hongyan Qiu
Language: English
Subfield: Clinical Biochemistry
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7123353971
