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Its main mechanism of action lies in inhibiting the TGF-1/Smad3 signaling pathway, thereby reducing the production of ROS, inhibiting the activation of hepatic stellate cells, reducing collagen synthesis, and delaying the progression of fibrosis

In vivo models showed that RBC@SeMSN@Uri effectively reduces uric acid levels and alleviates symptoms of hyperuricemia and gout, with prolonged circulation and targeted biodistribution

Gut-derived metabolites, such as short-chain fatty acids (SCFAs), bile acids, secondary bile acids, serotonin, taurine, glycerophospholipids, carboxylic acids and derivatives, fatty acyls, trimethylamine etc., were also observed to participate in the progression of ALD [119, 125, 139141]

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a low turnover rate in comparison with other immune cells (granulocytes, monocytes, and nave B cells), despite less turnover of other cells in the central nervous system (CNS