Targeting TGR5 to mitigate liver fibrosis: Inhibition of hepatic stellate cell activation through modulation of mitochondrial fission.

Chronic hepatitis B virus (HBV) infection continues to be a prominent cause of liver fibrosis and end-stage liver disease in China, necessitating the development of effective therapeutic strategies. This study investigated the potential of targeting TGR5 to alleviate liver fibrosis by impeding the activation of hepatic stellate cells (HSCs), which play a pivotal role in fibrotic progression. Using the human hepatic stellate cell line LX-2 overexpressing hepatitis B virus X protein (HBX), this study revealed that TGR5 activation through INT-777 inhibits HBX-induced LX-2 cell activation, thereby ameliorating liver fibrosis, which is associated with the attenuation of mitochondrial fission and introduces a novel regulatory pathway in liver fibrosis.

Differential developmental blueprints of organ-intrinsic nervous systems.

The organ-intrinsic nervous system is a major interface between visceral organs and the brain, mediating important sensory and regulatory functions in the body-brain axis and serving as critical local processors for organ homeostasis. Molecularly, anatomically, and functionally, organ-intrinsic neurons are highly specialized for their host organs. However, the underlying mechanism that drives this specialization is largely unknown.

New approach to establish a surgical planning in infantile vallecular cyst synchronous with laryngomalacia based on aerodynamic analysis.

Background And Objectives: A large proportion of infants with vallecular cyst (VC) have coexisting laryngomalacia (LM). Feeding difficulties, regurgitation, occasional cough, and sleep-disordered breathing are the common symptoms in moderate to severe cases. The surgical management of these cases is more challenging and remains controversial.