Analysis of the mechanism of action and anti-fibrosis principle of pirfenidone (Asri)

Pirfenidone (Pirfenidone) is an oral small molecule drug mainly used to treat idiopathic pulmonary fibrosis (IPF) and other fibrosis-related diseases. Its core mechanism of action is dual anti-inflammatory and anti-fibrotic effects, interfering with the fibrosis process through multiple signaling pathways, thereby delaying the structural destruction and functional decline of lung tissue.

Pirfenidone can inhibit the expression and activity of profibrotic factors such as transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF). TGF-β is a key driving molecule for fibrosis formation. It can promote fibroblast proliferation, collagen deposition and extracellular matrix remodeling. Pirfenidone reduces the activation of fibroblasts by downregulating TGF-β signaling, thereby inhibiting the excessive accumulation of collagen and fibrin.

Pirfenidone has anti-inflammatory effects and can reduce the levels of inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin -1β (IL-1β), etc. Inflammatory response is an important cause of early fibrosis. By inhibiting inflammatory cell infiltration and the release of inflammatory factors, pirfenidone can indirectly reduce the process of fibrosis and delay lung tissue hardening and functional decline.

Pirfenidone can also regulate oxidative stress and signaling pathways, such as inhibiting the generation of reactive oxygen species (ROS) and interfering with downstream signaling pathways such as MAPK and Smad, thereby reducing the pathological progression of fibrosis at multiple levels. Taken together, pirfenidone forms a multi-target anti-fibrosis network by inhibiting pro-fibrotic factors, reducing inflammatory responses and regulating oxidative stress, thereby achieving therapeutic effects of delaying disease progression and improving lung function.

Reference materials:https://www.drugs.com/