Researchers have identified how hydrogen sulfide may restrain oxidative stress, inflammation and abnormal smooth muscle cell growth linked to blood-vessel damage in type 2 diabetes.
Researchers have identified a molecular route by which hydrogen sulfide may help protect blood vessels in type 2 diabetes, adding fresh detail to a long-running effort to understand why diabetic vasculopathy develops and how it might be slowed. In work published in Cell Death Discovery, the team found that diabetic conditions reduced the activity of cystathionine γ-lyase, an enzyme that helps generate hydrogen sulfide, while also increasing oxidative stress, inflammation and the abnormal growth and movement of vascular smooth muscle cells.
The study used mice with type 2 diabetes and mouse aortic vascular smooth muscle cells exposed to high-glucose and high-fat conditions. Under those settings, the cells became more proliferative and more migratory, both features linked to vascular remodelling and vessel damage. Treatment with the hydrogen sulphide donor NaHS reversed much of that effect, suggesting that the gasotransmitter can counter some of the cellular changes associated with diabetic blood-vessel disease.
A key part of the mechanism appears to involve thioredoxin reductase 1, or TrxR1, an enzyme that helps control redox balance, the system by which cells manage oxidative stress. The researchers reported that hydrogen sulphide promoted a chemical modification known as S-sulfhydration on TrxR1, specifically at the Cys611 site, and that this changed the enzyme’s activity. That, in turn, influenced the Trx1-TXNIP-NLRP3 signalling pathway, which is closely tied to inflammatory activation. By damping this axis, hydrogen sulphide reduced inflammasome activity and eased the inflammatory and oxidative burden in the vessel cells.
The findings fit with earlier research portraying hydrogen sulphide as a vasculoprotective molecule. Reviews in BioMed Research International and The Scientific World Journal have described its antioxidant, anti-inflammatory and anti-proliferative effects, while separate studies have linked it to protection against diabetic kidney and heart damage through redox and inflammasome-related pathways. The new work extends that literature by connecting hydrogen sulphide more specifically to diabetic vascular smooth muscle behaviour, a process also shaped by hyperglycaemia, advanced glycation end products and other signalling changes known to drive macrovascular disease in type 2 diabetes.
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