RESUMO
A common denominator of metabolic diseases, including type 2 diabetes Mellitus, dyslipidemia, and atherosclerosis, are elevated oxidative stress and chronic inflammation. These complex, multi-factorial diseases are caused by the detrimental interaction between the individual genetic background and multiple environmental stimuli. The cells, including the endothelial ones, acquire a preactivated phenotype and metabolic memory, exhibiting increased oxidative stress, inflammatory gene expression, endothelial vascular activation, and prothrombotic events, leading to vascular complications. There are different pathways involved in the pathogenesis of metabolic diseases, and increased knowledge suggests a role of the activation of the NF-kB pathway and NLRP3 inflammasome as key mediators of metabolic inflammation. Epigenetic-wide associated studies provide new insight into the role of microRNAs in the phenomenon of metabolic memory and the development consequences of vessel damage. In this review, we will focus on the microRNAs related to the control of anti-oxidative enzymes, as well as microRNAs related to the control of mitochondrial functions and inflammation. The objective is the search for new therapeutic targets to improve the functioning of mitochondria and reduce oxidative stress and inflammation, despite the acquired metabolic memory.
RESUMO
We present a case of septicaemia caused by Arcanobacterium haemolyticum in a previously healthy 23-year-old man suffering from acute pharyngotonsillitis, who developed complicated Lemierre's syndrome. Three blood cultures (both aerobic and anaerobic) revealed the exclusive presence of A. haemolyticum. The presence of Fusobacterium necroforum was not essential for the development of this pathology. To our knowledge, this is the first reported case of Lemierre's syndrome caused solely by A. haemolyticum. We confirm that this organism must be considered a potential pathogen in immunocompetent patients.
