MicroRNAs (miRNAs) have received most of the attention over the last decades in particular for their role in tempering gene expression. An increasing number of studies highlighting the importance of miRNAs in the development and progression of atherosclerosis have been performed. Recently, it was shown that miRNAs exert their role in the pathophysiology of atherosclerosis via the regulation of atherosclerosis-prone genes as well as their impact in regulating post-transcriptional gene expression. Hence, by affecting the level of synthesised protein within cells, they may be significant in driving the dysregulation that affects endothelial cells, smooth muscle cells and leukocytes, which initiates and augments the growth of an atherosclerotic plaque. Furthermore, the circulating levels of vascular cell-enriched miRNAs in patients could serve as a marker of disease severity and phenotypes. The accumulating evidence also indicates that their effects on atherosclerosis may allow us to exploit miRNAs as novel therapeutics or clinical biomarkers that may lead to better management of vascular diseases. Current reports providing insights into the impact of miRNAs and the mechanisms of their influences in atherosclerosis are reviewed here with a particular emphasis on studies that have been recently published in Arteriosclerosis, Thrombosis, and Vascular Biology.

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The inhibition of amyloid‐β (Aβ) aggregation by photo‐oxygenation has become an effective way of treating Alzheimer's disease (AD). New near‐infrared (NIR) activated treatment agents, which not only possess high photo‐oxygenation efficiency, but also show low biotoxicity, are urgently needed. Herein, for the first time, it is demonstrated that NIR activated black phosphorus (BP) could serve as an effective nontoxic photo‐oxidant for amyloid‑β peptide in vitro and in vivo. The nanoplatform BP@BTA (BTA: one of thioflavin‐T derivatives) possesses high affinity to the Aβ peptide due to specific amyloid selectivity of BTA. Importantly, under NIR light, BP@BTA can significantly generate a high quantum yield of singlet oxygen (1O2) to oxygenate Aβ, thereby resulting in inhibiting the aggregation and attenuating Aβ‐induced cytotoxicity. In addition, BP could finally degrade into nontoxic phosphate, which guarantees the biosafety. Using transgenic Caenorhabditis elegans CL2006 as AD model, the results demonstrate that the 1O2‐generation system could dramatically promote life‐span extension of CL2006 strain by decreasing the neurotoxicity of Aβ.

Phenotyping of Gprc6a KO mice has shown that this promiscuous class C G protein coupled receptor is variously involved in regulation of metabolism, inflammation and endocrine function. Such effects are described as mediated by extracellular calcium, L-amino acids, the bone-derived peptide osteocalcin (OCN) and the male hormone testosterone, introducing the concept of a bone-energy-metabolism-reproduction functional crosstalk mediated by GPRC6A. However, whilst the calcium and L-amino acid-sensing properties of GPRC6A are well established, verification of activity of osteocalcin at both human and mouse GPRC6A in vitro has proven somewhat elusive. This study characterises the in vitro pharmacology of mouse GPRC6A in response to its putative ligands in both recombinant and endogenous GPRC6A-expressing cells. Using cell signalling, and glucagon-like peptide (GLP)-1 and insulin release assays, our results confirm that basic L-amino acids act as agonists of the murine GPRC6A receptor in both recombinant cells and immortalised entero-endocrine and pancreatic β-cells. In contrast, our studies do not support a role for OCN as a direct ligand for mouse GPRC6A, suggesting that the reported in vivo effects of OCN that require GPRC6A may be indirect, rather than via direct activation of the receptor.

Background To compare the clinical efficacy of a femoral neck system (FNS) and cannulated screws (CS) in the treatment of femoral neck fracture in young adults. Methods Data from 69 young adults, who were admitted for femoral neck fracture between March 2018 and June 2020, were retrospectively analyzed. Patients were divided into two groups according to surgical method: FNS and CS. The number of intraoperative fluoroscopies, operative duration, length of hospital stay, fracture healing time, Harris score of hip function, excellent and good rate of hip function, and postoperative complications (infection, cut out the internal fixation, nail withdrawal, and femoral neck shortening) were compared between the two groups. Hip joint function was evaluated using the Harris Hip Scoring system. Results All 69 patients had satisfactory reduction and were followed up for 12–24 months, with a mean follow-up of 16.91 ± 3.01 months. Mean time to fracture healing was13.82 ± 1.59 and 14.03 ± 1.78 weeks in the FNS and CS groups, respectively. There was a statistical difference in the number of intraoperative fluoroscopies between the 2 groups (P = 0.000). There were no significant differences, in operation duration, hospital length of stay, fracture healing time, complications, Harris Hip Score for hip function and excellent and good rate between the two groups (P > 0.05). The incidence of complications was 6.1%(2/33) in the FNS group lower than 25%(9/36) in the CS group, a difference that was statistically significant (P = 0.032). At the last follow-up, the Harris Hip Score of the hip joint in the FNS group was 90.42 ± 4.82and 88.44 ± 5.91 in the CS group. Conclusions Both treatment methods resulted in higher rates of fracture healing and excellent hip function. Compared with CS, the FNS reduced the number of intraoperative fluoroscopies, radiation exposure to medical staff and patients, and short-term complications including femoral neck shortening and bone nonunion.