Bruce D. Hammock

This study shows that inhibiting soluble epoxide hydrolase with TPPU improves cognitive function in diabetic-related dementia by enhancing cerebral blood flow and reducing neuroinflammation and gliosis.

This study identifies CES1 deficiency as a driver of metabolic reprogramming and endothelial dysfunction in pulmonary arterial hypertension, showing its role in lipid metabolism and oxidative stress.

This study shows that soluble epoxide hydrolase in astrocytes contributes to vascular instability in Alzheimer's disease, and its deletion reduces vascular amyloid burden and preserves vascular structure.

This study shows that dual inhibition of sEH and COX-2 with PTUPB improves cognition in AD rats by enhancing myogenic response and cerebral artery distensibility.

This study shows that inhibiting soluble epoxide hydrolase reduces inflammation and myocardial injury in arrhythmogenic cardiomyopathy by increasing pro-resolving lipid mediators.

This study shows that inhibiting soluble epoxide hydrolase (sEH) with TPPU improves cerebral blood flow autoregulation and cognition in Alzheimer's and diabetes-related dementia rat models.

This paper develops next-generation sEH-targeting PROTACs with improved potency and stability, showing effective degradation in mouse tissues.

This study shows that P2-HNF4 regulates ketogenesis in the liver and is involved in circadian metabolism, with implications for gender-specific ketone body levels.

The paper identifies EPHX1 mutations causing lipoatrophic diabetes through impaired epoxide hydrolysis and increased cellular senescence, with metreleptin therapy showing benefit.

The paper shows that soluble epoxide hydrolase is upregulated in AD and that its inhibition restores brain epoxy fatty acids, ameliorates neuropathology, and improves cognitive function.