The role of High Mobility Group Box Protein 1 (HMGB1) is increasingly emerging in diabetes-associated complications, particularly diabetic encephalopathy (DE) and diabetic kidney disease (DKD). As a pro-inflammatory molecule released during cellular stress, HMGB1 acts as a damage-associated molecular pattern (DAMP) to propagate inflammatory pathways, which may exacerbate diabetes complications.
HMGB1 role in Diabetic Encephalopathy
HMGB1’s release is known to contribute to cognitive decline in diabetes. Through interaction with receptors such as RAGE and toll-like receptors (TLR), HMGB1 promotes neuroinflammation, disrupts the blood-brain barrier, and increases oxidative stress, all contributing to neuronal damage and cognitive impairment. This role underscores its potential as a therapeutic target in managing diabetes-induced neurodegeneration.
HMGB1 as a Biomarker for Diabetic Kidney Disease (DKD)
HMGB1 also shows strong potential as a biomarker in diabetic kidney disease, a common and severe complication in type 2 diabetes. Research reveals that serum and urine levels of HMGB1 are significantly elevated in patients with DKD, correlating with markers of renal function decline, including TNFR-1 and KIM-1.
Notably, when serum HMGB1 levels exceed a threshold (≥27 ng/mL), the risk of DKD progression increases sharply, positioning HMGB1 as a reliable biomarker for tracking kidney disease severity and progression in diabetes patients. Detecting elevated HMGB1 could enable earlier interventions to slow DKD’s course.
By targeting HMGB1, there is potential to mitigate inflammation-driven damage in both neural and renal tissues, offering new avenues in diabetes care.
In HMGBiotech SRL we provide a suite of research-grade HMGB1 products to facilitate further investigation into its roles and therapeutic potential.
Contact us for your pre-sales questions about HMGB1
Read the full articles about the studies:
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1334109/full
https://link.springer.com/article/10.1007/s12035-024-04081-z
