Proteins mediating collagen biosynthesis and accumulation in arterial repair: novel targets for anti-restenosis therapy

• Published in: Cardiovascular research Vol. 91; no. 1; pp. 16 - 26
• Main Authors: Osherov, Azriel B., Gotha, Lara, Cheema, Asim N., Qiang, Beiping, Strauss, Bradley H.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.07.2011
• Subjects: Angioplasty, Balloon, Coronary - adverse effects; Angioplasty, Balloon, Coronary - instrumentation; Animals; Biological and medical sciences; Cardiology. Vascular system; Cardiovascular Agents - pharmacology; Collagen - biosynthesis; Collagen - metabolism; Collagenases - metabolism; Coronary Restenosis - etiology; Coronary Restenosis - metabolism; Coronary Restenosis - prevention & control; Coronary Stenosis - therapy; Cytokines - antagonists & inhibitors; Cytokines - metabolism; Diseases of the cardiovascular system; Enzyme Inhibitors - pharmacology; Humans; Integrins - antagonists & inhibitors; Integrins - metabolism; Intercellular Signaling Peptides and Proteins - metabolism; Matrix Metalloproteinase Inhibitors; Medical sciences; Protein-Lysine 6-Oxidase - antagonists & inhibitors; Protein-Lysine 6-Oxidase - metabolism; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); Signal Transduction - drug effects; Stents; Extracellular matrix; Extracellular response; Balloon angioplasty and stenting; Collagen synthesis and processing; Corrective surgery; Angioplasty; Targeted therapy; Instrumentation therapy; Biosynthesis; Instrumental dilatation; Extracellular; Phlebology; Stent; Accumulation; Artery; Protein; Restenosis; Response; Synthesis; Collagen; Circulatory system; Cardiology; Repair
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1093/cvr/cvr012

Events contributing to restenosis after coronary interventions include platelet aggregation, inflammatory cell infiltration, growth factor release, and accumulation of smooth muscle cells (SMCs) and extracellular matrix (ECM). The ECM is composed of various collagen subtypes and proteoglycans and over time constitutes the major component of the mature restenotic plaque. The pathophysiology of collagen accumulation in the ECM during arterial restenosis is reviewed. Factors regulating collagen synthesis and degradation, including various cytokines and growth factors involved in the process, may be targets for therapies aimed at prevention of in-stent restenosis.