Vascular calcification (VC) is considered a common pathological process in various vascular diseases. Accumulating studies have confirmed that VC is involved in the inflammatory response in heart disease, and SPP1+ macrophages play an important role in this process. In VC, studies have focused on the physiological and pathological functions of macrophages, such as pro-inflammatory or anti-inflammatory cytokines and pro-fibrotic vesicles. Additionally, macrophages and activated lymphocytes highly express SPP1 in atherosclerotic plaques, which promote the formation of fatty streaks and plaque development, and SPP1 is also involved in the calcification process of atherosclerotic plaques that results in heart failure, but the crosstalk between SPP1-mediated immune cells and VC has not been adequately addressed. In this review, we summarize the regulatory effect of SPP1 on VC in T cells, macrophages, and dendritic cells in different organs’ VC, which could be a potential therapeutic target for VC.

In contrast to polymer bioresorbable stents (BRS) that exhibited suboptimal performance in clinical trials due to their deficient mechanical properties, metallic BRS with improved mechanical strength have made their way into the clinic and have demonstrated more promising results. In the roadmap of research and development of metallic BRS, magnesium and iron based biodegradable metal stents had been clinically used, and the zinc based biodegradable metal stents had been trailed in Mini-Pigs. In this mini-review paper, we demonstrate the current technology levels and point out the future R&D direction of metallic BRS. Magnesium based BRS should target for decreasing struct thickness meanwhile balancing with enough supporting strength. Iron based BRS should move towards high efficient absorption, conversion, metabolism, elimination of its degradation products. Zn based BRS should strive to improve mechanical stability, creep resistance and biocompatibility. Future R&D directions of metallic BRS should move towards new materials such as Molybdenum, intelligent stent integrated with degradable biosensors, and new stent with multiple biofunctions, such as NO release.

Rhodiola algida var. tangutica is a traditional Tibetan herb. Its root and rhizome have been successfully used as an effective clinical remedy for the prevention and treatment of cancer and high-altitude sickness. This study aimed to investigate the effect of Rhodiola algida var. tangutica on hypoxic MCF-7 breast cancer cells and the underlying mechanisms. The antiproliferative effects of R. algida on MCF-7 breast cancer cells were compared in vitro under hypoxic and normal conditions by using MTT analysis. The influence of R. algida on cancer cell apoptosis was determined by flow cytometry. The expression levels of hypoxia-inducible factor (HIF)-1α and HIF-2α were evaluated by western blot analysis. R. algida inhibited the proliferation of MCF-7 breast cancer cells in a dose- and time-dependent manner. The results of flow cytometry indicated that the antiproliferative effect of R. algida was mediated by apoptosis induction. Pretreatment with R. algida significantly suppressed the hypoxia-induced proliferation and expression of HIF-1α and HIF-2α in MCF-7 breast cancer cells. R. algida might exert an anti-carcinogenic effect on MCF-7 breast cancer cells by decreasing the protein levels of HIF-1α and HIF-2α, which are overexpressed under hypoxic conditions. This effect might be elicited by inhibiting the hypoxia-induced proliferation of MCF-7 breast cancer cells.

Pulmonary hypertension (PH) is defined as the mean pulmonary artery pressure (mPAP) ≥25 mmHg under the sea level in resting state. ROCK1 and ROCK2 can be combined to cause the damage of vascular endothelial function. To explore the differences of ROCK1 and ROCK2 in subjects with pulmonary hypertension or normal pulmonary artery pressure in plateau area, and to further understand the mechanism of Rho/rho-kinase pathway activation for promoting pulmonary hypertension, we collected 64 patients with pulmonary hypertension and 87 normal pulmonary artery healthy controls. All subjects were hospitalized in Cardiology or Respiration Department of Qinghai Provincial Peoples’ Hospital from December 2016 to June 2017. The pulmonary artery systolic pressure was measured by Doppler ultrasound, and serum ROCK1 and ROCK2 levels were tested by enzyme linked immunosorbent assay (ELISA). We found that the serum ROCK2 concentration in the pulmonary hypertension group was significantly higher than that in the control group, but serum ROCK1 level had no significant difference. ROCK2 plays a leading role in pulmonary hypertension in the plateau region, so selective ROCK2 inhibitors will be more effective in improving pulmonary hypertension.