Aim To investigate the effect of store-oper-ated calcium channel( SOCC) on autophagy in rat arte-rial smooth muscle cells A7 R5 . Methods Lentiviruses containing STIM1 or Orai1 gene were packaged in 293 T cells and then were used to infect rat arterial smooth muscle cells A7 R5 . The expression levels of STIM1 , Orai1 and Beclin 1 , a critical autophagy-regu-lating protein, of lentivirus-infected A7R5 cells, were detected by Western-blot. Autophagy in lentivirus-in-fected A7 R5 cells was induced by starvation or rapamy-cin, an inhibitor of mammalian target of rapamycin ( mTOR ) . Autophagy marker LC3 of these cells was detected by Western-blot. Results The constructions of vector pLV-STIM1 and pLV-Orai1 were confirmed by restriction enzymes digestion analysis. Compared with the control group, expressions of STIM1 or Orai1 protein was significantly increased after lentivirusLV-STIM1 and LV-Orai1infection, whereas the expressions of autophagy related protein Beclin-1 were down-regu-lated. Starvation or rapamycin stimulated A7R5 auto-phagy but overexpression of STIM1 or Orai1 significant-ly inhibited starvation or rapamycin induced autoph-agy. Conclusion Overexpression of store-operated calcium channel components STIM1 and/or Orai1 in rat arterial smooth muscle cells A7 R5 inhibit autoph-agy. This mechanism might contribute to the develop-ment of pulmonary arterial hypertension.

Atherosclerosis （AS） is a chronic multifactorial vascular disease and a major pathological basis of cardiovascular diseases. It mainly occurs in the middle-aged and elderly and causes high mortality. Apoptosis is a form of spontaneous programmed death. Under pathological conditions， the apoptosis of vascular endothelial cells （VECs）， vascular smooth muscle cells （VSMCs）， and macrophages is the key factor of the occurrence and development of AS. The apoptosis of VECs may be an early event that promotes the formation and progression of AS lesions， while the subsequent apoptosis of VSMCs and macrophages accelerates the formation of AS unstable plaques and plays a key role in the late stage of AS. Therefore， apoptosis may provide a new target for the treatment of AS. Increasing evidence has demonstrated that Chinese medicine plays a positive role in the treatment of AS by regulating apoptosis factors and apoptosis-associated signaling pathways. However， the studies about the treatment of AS with Chinese medicine from apoptosis have not been systematically reviewed. Therefore， we reviewed the relevant literature and systematically summarized the molecular mechanisms of apoptosis. Specifically， we focused on mitochondrial apoptosis pathway， death receptor apoptosis pathway， endoplasmic reticulum stress apoptosis pathway and explored the role of apoptosis in AS. Further， we reviewed the progress in the role and mechanism of Chinese medicine in regulating apoptosis against AS， aiming to provide a theoretical basis for the treatment of AS and the development of drugs.