从气虚络瘀论特发性肺纤维化自噬机制

中医理论认为,特发性肺纤维化（idiopathic pulmonary fibrosis, IPF）的关键病机在于“气虚络瘀”。IPF患者自噬水平不足,不能及时清除异常病理物质,造成细胞外基质过度沉积而致肺纤维化。这与气虚无力推动新陈代谢,形成病理产物堆积,进而壅滞肺络,最终导致肺叶痿弱而不用相对应。因此,自噬不足导致的病理过程可视为“气虚络瘀”病机的微观机制,运用气虚络瘀理论阐释IPF自噬机制并通过调控自噬以防治本病可能成为新的重要靶点。

Autophagy Mechanism of Idiopathic Pulmonary Fibrosis from the Perspective of Qi Deficiency and Collateral Obstruction

Traditional Chinese medicine theory believes that Qi deficiency and collateral obstruction is the key pathogenesis of idiopathic pulmonary fibrosis (IPF). Due to insufficient autophagy in IPF patients, abnormal pathological substances cannot be cleared in time, leading to excessive deposition of extracellular matrix and thus pulmonary fibrosis. This is consistent with the theory that Qi deficiency cannot promote metabolism and thus pathological products accumulate and cause lung collateral obstruction, which finally leads to lung weakness. Therefore, the pathological process caused by insufficient autophagy can be regarded as the microscopic mechanism of the pathogenesis of "Qi deficiency and collateral obstruction", and explanation of the autophagy mechanism of IPF based on Qi deficiency and collateral obstruction and regulation of autophagy for the prevention and treatment of this disease may become a new important target.