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BRB disruption is a primary pathogenic mechanism of DR and the key factor driving DR progression from non-proliferative DR (NPDR) to proliferative DR (PDR)

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The BHBA-induced increase of p-CREB levels was inhibited by manidipine, suggesting that L-type VSCCs are responsible for the elevation of p-CREB induced by BHBA (Figure 4C)

doi: 10.2147/DDDT.S556231, Summary Keywords fibrosis, glucagon-like peptide-1 receptor agonists, inflammation, metabolic dysfunction-associated steatohepatitis, metabolic dysfunction-associated steatotic liver disease Citation Lu X and Yang L (2026) Glucagon-like peptide-1 and dual/triple receptor agonists in the treatment of metabolic dysfunction-associated steatotic liver disease: advances in mechanistic research