The arterial adventitia has been long considered an essentially supportive tissue; however, more and more data suggest that it plays a major role in the modulation of the vascular tone by complex interactions with structures located within intima and media. The purpose of this review is to summarize these data and to describe the mechanisms involved in adventitia/media and adventitia/intima cross-talk. In response to a plethora of stimuli, the adventitia undergoes remodeling processes, resulting in positive (adaptive) remodeling, negative (constrictive) remodeling, or both. The differentiation of the adventitial fibroblast into myofibroblast (MF), a key player of wound healing and fibrosis development, is a hallmark of negative remodeling; this can lead to vessel stenosis and thus contribute to major cardiovascular diseases. The mechanisms of fibroblast-to-MF differentiation and the role of the MF in adventitial remodeling are highlighted herein.

It is well accepted that LDLs and its modified form oxidized-LDL (ox-LDL) play a major role in the development of atherosclerosis and foam cell formation. Whereas the majority of these cells have been demonstrated to be derived from macrophages, smooth muscle cells (SMCs) give rise to a significant number of foam cells as well. During atherosclerotic plaque formation, SMCs switch from a contractile to a synthetic phenotype. The contribution of this process to foam cell formation is still not well understood. It has been confirmed that a large proportion of foam cells in human atherosclerotic plaques and in experimental intimal thickening arise from SMCs. SMC-derived foam cells express receptors involved in ox-LDL uptake and HDL reverse transport. In-vitro studies show that treatment of SMCs with ox-LDL induces typical foam-cell formation; this process is associated with a transition of SMCs toward a synthetic phenotype. This review summarizes data regarding the phenotypic switch of arterial SMCs within atherosclerotic lesion and their contribution to intimal foam cell formation.

There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, even in its mild or moderate respiratory forms, can include long-term neuropsychological deficits. Standardized neuropsychological, psychiatric, neurological, and olfactory tests were administered to 45 patients 236.51 ± 22.54 days after hospital discharge following severe, moderate, or mild respiratory severity from SARS-CoV-2 infection (severe = intensive care unit hospitalization, moderate = conventional hospitalization, mild = no hospitalization). Deficits were found in all domains of cognition, and the prevalence of psychiatric symptoms was relatively high in the three groups. The severe infection group performed more poorly on long-term episodic memory tests and exhibited greater anosognosia than did the other two groups. Those with moderate infection had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. Individuals with mild infection were more stressed, anxious, and depressed. The data support the hypothesis that the virus targets the central nervous system (notably the limbic system) and the notion that there are different neuropsychological phenotypes.