title: Heme oxygenase-1 and the vascular bed: from molecular mechanisms to therapeutic opportunities.
abstract: Heme oxygenase-1, an enzyme degrading heme to carbon monoxide, iron, and biliverdin, has been recognized as playing a crucial role in cellular defense against stressful conditions, not only related to heme release. HO-1 protects endothelial cells from apoptosis, is involved in blood-vessel relaxation regulating vascular tone, attenuates inflammatory response in the vessel wall, and participates in blood-vessel formation by means of angiogenesis and vasculogenesis. The latter functions link HO-1 not only to cardiovascular ischemia but also to many other conditions that, like development, wound healing, or cancer, are dependent on neovascularization. The aim of this comprehensive review is to address the mechanisms of HO-1 regulation and function in cardiovascular physiology and pathology and to demonstrate some possible applications of the vast knowledge generated so far. Recent data provide powerful evidence for the involvement of HO-1 in the therapeutic effect of drugs used in cardiovascular diseases. Novel studies open the possibilities of application of HO-1 for gene and cell therapy. Therefore, research in forthcoming years should help to elucidate both the real role of HO-1 in the effect of drugs and the clinical feasibility of HO-1-based cell and gene therapy, creating the effective therapeutic avenues for this refined antioxidant system.
authors.affiliation: Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Loboda
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Jazwa
authors.forename: Anna
authors.initials: A
authors.lastname: Grochot-Przeczek
authors.forename: Andrzej J
authors.initials: AJ
authors.lastname: Rutkowski
authors.forename: Jaroslaw
authors.initials: J
authors.lastname: Cisowski
authors.forename: Anupam
authors.initials: A
authors.lastname: Agarwal
authors.forename: Alicja
authors.initials: A
authors.lastname: Jozkowicz
authors.forename: Jozef
authors.initials: J
authors.lastname: Dulak
mesh_terms: D000818:Animals; D017209:Apoptosis; D001664:Biliverdine / Q000378:metabolism; D002248:Carbon Monoxide / Q000378:metabolism / Q000494:pharmacology / Q000633:toxicity; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000201:enzymology / Q000628:therapy; D002648:Child; D048909:Diabetes Complications / Q000201:enzymology / Q000517:prevention & control / Q000628:therapy; D004730:Endothelium, Vascular / Q000201:enzymology*; D004790:Enzyme Induction / Q000187:drug effects / Q000528:radiation effects; D005260:Female; D015316:Genetic Therapy; D006418:Heme / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000737:chemistry / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000628:therapy; D007501:Iron / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D018919:Neovascularization, Physiologic; D011817:Rabbits; D051381:Rats; D014666:Vasomotor System / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents; D006418:Heme; D002248:Carbon Monoxide; D007501:Iron; D051547:Heme Oxygenase-1; D001664:Biliverdine