Commentary on: Physalin B attenuates liver fibrosis via suppressing LAP2α-HDAC1 mediated deacetylation of GLI1 and hepatic stellate cell activation

Liver fibrosis is an excessive scarring process resulting in progressive disruption of the normal tissue architecture and impaired organ function. It comprises many different etiologies and its consequences present a substantial medical and economic burden worldwide Mechanistically, fibrosis is initiated by parenchymal cell destruction resulting in tissue damage that is associated with an inflammatory response. This in turn provokes the local activation of mesenchymal cells which have the capacity to produce extracellular matrix compounds such as collagens. Most important in this process are hepatic stellate cells (HSCs) that are pericytes in the perisinusoidal space of the liver. Upon activation, these cells lose their quiescent phenotype and transit in a process called transdifferentiation into proliferative fibrogenic -smooth muscle positive (-SMA) myofibroblasts. These are the central cellular drivers of hepatic fibrogenesis in experimental and human liver injury. Although the cellular and molecular mechanisms of hepatic fibrosis including important pro-inflammatory and pro-fibrogenic soluble mediators (chemokines, cytokines) and signaling pathways are identified, there exist no specific and effective antifibrotic pharmacological therapies.