myricetin

Overview

Myricetin is a naturally occurring flavonoid that has attracted attention in biomedical research for its potential anti-inflammatory, antiviral, and cardiometabolic effects. In the recent literature provided here, it is discussed primarily as a bioactive small molecule rather than as a gene product, with studies examining its interactions with disease-relevant proteins and signaling pathways.

Across these reports, myricetin is associated with modulation of cellular stress responses and disease-associated signaling, including ferroptosis-related SLC7A11/GPX4 signaling in vascular calcification and direct targeting of HSV gD protein in herpes infection models. It has also been described in the context of flavonoid-rich plant extracts alongside quercetin, rutin, luteolin, and isorhamnetin, underscoring its role as one of several structurally related natural compounds of pharmacological interest.

Focus of Latest Publications

Recent investigations have examined myricetin, a natural flavonoid, across three distinct disease contexts: intestinal aging, diabetic vascular complications, and viral infection. In a lipopolysaccharide-induced intestinal aging model using engineered organoids, myricetin effectively suppressed age-related pathology by inhibiting NF-κB activation and reducing proinflammatory cytokines. Transcriptomic analysis revealed that myricetin's antiaging effects involve modulation of the MAPK, PI3K/Akt, and NF-κB signaling pathways, positioning it as a candidate for screening additional traditional Chinese medicine-derived antiaging compounds.

In the context of diabetic vascular disease, myricetin demonstrated protective effects in vascular smooth muscle cells exposed to hyperglycemic and phosphate conditions in vitro. The compound attenuated osteogenic transdifferentiation by decreasing RUNX2 and BMP-2 expression while restoring contractile phenotype markers α-SMA and SM22-α. Additionally, myricetin reduced oxidative stress through decreased Intracellular ROS and malondialdehyde levels and restored expression of ferroptosis regulators including SLC7A11, GPX4, and FTH1, suggesting a mechanism involving ferroptosis modulation. These findings indicate therapeutic potential for preventing vascular calcification in type 2 diabetes mellitus.

For viral infection, myricetin was evaluated against herpes simplex virus type 2, where computational and experimental evidence demonstrated its ability to bind the viral gD glycoprotein. To overcome the compound's limited aqueous solubility, researchers encapsulated myricetin into polycarboxylate nanoparticles and formulated an in-situ gelling preparation for intravaginal delivery. In a murine model of genital herpes, the myricetin-nanoparticle formulation demonstrated superior antiviral efficacy compared to free myricetin solution, suggesting that appropriate delivery strategies may enhance its bioavailability and clinical utility against HSV-2 infection.