title: Novel potential targets for prevention of arterial restenosis: insights from the pre-clinical research.
abstract: Restenosis is the pathophysiological process occurring in 10-15% of patients submitted to revascularization procedures of coronary, carotid and peripheral arteries. It can be considered as an excessive healing reaction of the vascular wall subjected to arterial/venous bypass graft interposition, endarterectomy or angioplasty. The advent of bare metal stents, drug-eluting stents and of the more recent drug-eluting balloons, have significantly reduced, but not eliminated, the incidence of restenosis, which remains a clinically relevant problem. Biomedical research in pre-clinical animal models of (re)stenosis, despite its limitations, has contributed enormously to the identification of processes involved in restenosis progression, going well beyond the initial dogma of a primarily proliferative disease. Although the main molecular and cellular mechanisms underlying restenosis have been well described, new signalling molecules and cell types controlling the progress of restenosis are continuously being discovered. In particular, microRNAs and vascular progenitor cells have recently been shown to play a key role in this pathophysiological process. In addition, the advanced highly sensitive high-throughput analyses of molecular alterations at the transcriptome, proteome and metabolome levels occurring in injured vessels in animal models of disease and in human specimens serve as a basis to identify novel potential therapeutic targets for restenosis. Molecular analyses are also contributing to the identification of reliable circulating biomarkers predictive of post-interventional restenosis in patients, which could be potentially helpful in the establishment of an early diagnosis and therapy. The present review summarizes the most recent and promising therapeutic strategies identified in experimental models of (re)stenosis and potentially translatable to patients subjected to revascularization procedures.
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Amalia
authors: A
authors: Forte
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Barbara
authors: B
authors: Rinaldi
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Liberato
authors: L
authors: Berrino
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Francesco
authors: F
authors: Rossi
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Umberto
authors: U
authors: Galderisi
authors: *Department of Experimental Medicine, Second University of Naples, Via L. De Crecchio 7, 80138 Naples, Italy.
authors: Marilena
authors: M
authors: Cipollaro
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D023903:Coronary Restenosis / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D015316:Genetic Therapy; D008297:Male; D051379:Mice; D035683:MicroRNAs / Q000502:physiology; D023421:Models, Animal; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D011183:Postoperative Complications / Q000188:drug therapy / Q000517:prevention & control; D017208:Rats, Wistar; D012038:Regeneration; D013234:Stem Cells / Q000502:physiology
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D035683:MicroRNAs