FNDC5/irisin-enriched sEVs conjugated with bone-targeting aptamer alleviate osteoporosis: a potential alternative to exercise.

Exercise maintains bone health and produces protective effects on bone loss. In this study, we investigated the potential protective effects of circulating small extracellular vesicles (sEVs) generated under endurance exercise training (Exe-sEVs) on ovariectomized (OVX)-induced bone loss. Inhibition of sEVs secretion by GW4869 partially reversed exercised-induced protection against OVX-induced bone loss.

Erdheim-Chester disease with asymmetric talus involvement: A case report.

Background: Erdheim-Chester disease (ECD) is a rare multi-system or multi-organ histiocytic proliferative disease with diverse clinical manifestations, and the development of the disease is complex, which makes clinical diagnosis and treatment difficult. The characteristic clinical manifestations include multi-organ involvement, especially in the symmetrical diaphysis and metaphysis of the bilateral extremities. ECD with a unilateral talus lesion is extremely rare.

Arterial Calcification Is Regulated Via an miR-204/DNMT3a Regulatory Circuit Both In Vitro and in Female Mice.

Arterial calcification is a common cardiovascular disease that initiates from a process of osteoblastic differentiation of vascular smooth muscle cells (VSMCs). Accumulating evidence has demonstrated that microRNAs play an important role in regulating arterial calcification. miR-204 was significantly downregulated in calcified human renal arteries from patients with uremia; calcified arteries of mice, due to 5/6 nephrectomy with a high-phosphate diet (5/6 NTP); and in VSMCs induced by high phosphate concentration.

Oestrogen Inhibits Arterial Calcification by Promoting Autophagy.

Arterial calcification is a major complication of cardiovascular disease. Oestrogen replacement therapy in postmenopausal women is associated with lower levels of coronary artery calcification, but its mechanism of action remains unclear. Here, we show that oestrogen inhibits the osteoblastic differentiation of vascular smooth muscle cells (VSMCs) in vitro and arterial calcification in vivo by promoting autophagy.