The mechanisms underlying ageing-induced vascular remodelling remain unclear. This study investigates the role and underlying mechanisms of the cytoplasmic deacetylase sirtuin 2 (SIRT2) in ageing-induced vascular remodelling. Transcriptome and quantitative real-time PCR data were used to analyse sirtuin expression. Young and old wild-type and Sirt2 knockout mice were used to explore vascular function and pathological remodelling. RNA-seq, histochemical staining, and biochemical assays were used to evaluate the effects of Sirt2 knockout on the vascular transcriptome and pathological remodelling and explore the underlying biochemical mechanisms. Among the sirtuins, SIRT2 had the highest levels in human and mouse aortas. Sirtuin 2 activity was reduced in aged aortas, and loss of SIRT2 accelerated vascular ageing. In old mice, SIRT2 deficiency aggravated ageing-induced arterial stiffness and constriction–relaxation dysfunction, accompanied by aortic remodelling (thickened vascular medial layers, breakage of elastin fibres, collagen deposition, and inflammation). Transcriptome and biochemical analyses revealed that the ageing-controlling protein p66^Shc and metabolism of mitochondrial reactive oxygen species (mROS) contributed to SIRT2 function in vascular ageing. Sirtuin 2 repressed p66^Shc activation and mROS production by deacetylating p66^Shc at lysine 81. Elimination of reactive oxygen species by MnTBAP repressed the SIRT2 deficiency–mediated aggravation of vascular remodelling and dysfunction in angiotensin II–challenged and aged mice. The SIRT2 coexpression module in aortas was reduced with ageing across species and was a significant predictor of age-related aortic diseases in humans. The deacetylase SIRT2 is a response to ageing that delays vascular ageing, and the cytoplasm–mitochondria axis (SIRT2–p66^Shc–mROS) is important for vascular ageing. Therefore, SIRT2 may serve as a potential therapeutic target for vascular rejuvenation. The epigenetic regulator sirtuin 2 (SIRT2) governs a cytoplasm–mitochondria signal to repress vascular ageing. Ageing reduces SIRT2 protein levels and activity, which results in the hyperacetylation and activation of the adaptor protein p66^Shc and production of mitochondrial reactive oxygen species (mROS), which subsequently reprogrammes the vascular transcriptome to aggravate ageing-induced vascular remodelling and diseases. The circulating SIRT2 may serve as a prognostic biomarker for ageing-related vascular diseases, and the cytoplasm–mitochondria axis SIRT2–p66^Shc–mROS could be targeted for treating ageing-related vascular diseases.

Multiple radar systems represent an attractive option for target tracking because they can significantly enlarge the area coverage and improve both the probability of trajectory detection and the localization accuracy. The presence of multiple extended targets or weak targets is a challenge for multiple radar systems. Moreover, their performance may be severely deteriorated by regions characterized by a high clutter density. In this article, an algorithm for detection and tracking of multiple targets, extended or weak, based on measurements provided by multiple radars in an environment with heavily cluttered regions, is proposed. The proposed method features three stages. In the first stage, past measurements are exploited to build a spatiotemporal clutter map in each radar; a weight is then assigned to each measurement to assess its significance. In the second stage, a track-before-detect algorithm, based on a weighted 3-D Hough transform, is applied to obtain target tracklets. In the third stage, a low-complexity tracklet association method, exploiting a lion reproduction model, is applied to associate tracklets of the same target. Three experiments are presented to illustrate the effectiveness of the proposed approach. The first experiment is based on synthetic data, the second one is based on actual data from a radar network with two homogeneous air surveillance radars, and the third one is based on actual data from a radar network with four different marine surveillance radars. The results reveal that the proposed method can outperform competing approaches.

The ocular tissue microenvironment is immune-privileged and uses multiple immunosuppressive mechanisms to prevent the induction of inflammation. The retinal pigment epithelium plays an essential role in ocular immune privilege. In addition to serving as a blood barrier separating the fenestrated choriocapillaris from the retina, the retinal pigment epithelium is a source of immunosuppressive cytokines and membrane-bound negative regulators that modulate the activity of immune cells within the retina. This article reviews the current understanding of how retinal pigment epithelium cells mediate immune regulation, focusing on the changes under pathologic conditions.

Cardiovascular disease is still the main cause of morbidity and mortality worldwide. Currently, the frontier of research into cardiovascular disease is the field of non-coding RNA. In this review, information was collected on the use of micro-RNAs as non-invasive biomarkers and their role in pathophysiological processes and therapeutic applications. In the case of microRNA-1 and microRNA-133, the roles and regulatory mechanisms of them are reviewed for arrhythmia, myocardial infarction, diabetic cardiomyopathy, myocardial hypertrophy, cardiomyocyte differentiation, and cell reprogramming. It was observed that microRNA-1 and microRNA-133 do not exist independently, but are two co-transcriptional and cooperative regulatory factors. They have diagnostic value as biomarkers, but also have the potential as therapeutic targets such as for antiarrhythmia and cardiac reprogramming.