Pathogenetic role of eNOS uncoupling in cardiopulmonary disorders
Copyright © 2010. Published by Elsevier Inc..
The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation. Chronically, eNOS has a major role in the regulation of blood pressure and prevention of atherosclerosis by decreasing leukocyte adhesion and smooth muscle proliferation. However, a disturbed vascular redox balance results in eNOS damage and uncoupling of oxygen activation from l-arginine conversion. Uncoupled eNOS monomerizes and generates reactive oxygen species (ROS) rather than NO. Indeed, eNOS uncoupling has been suggested as one of the main pathomechanisms in a broad range of cardiovascular and pulmonary disorders such as atherosclerosis, ventricular remodeling, and pulmonary hypertension. Therefore, modulating uncoupled eNOS, in particular eNOS-dependent ROS generation, is an attractive therapeutic approach to preventing and/or treating cardiopulmonary disorders, including protective effects during cardiothoracic surgery. This review provides a comprehensive overview of the pathogenetic role of uncoupled eNOS in both cardiovascular and pulmonary disorders. In addition, the related therapeutic possibilities such as supplementation with the eNOS substrate l-arginine, volatile NO, and direct NO donors as well as eNOS modulators such as the eNOS cofactor tetrahydrobiopterin and folic acid are discussed in detail.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2011 |
|---|---|
| Erschienen: |
2011 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:50 |
|---|---|
| Enthalten in: |
Free radical biology & medicine - 50(2011), 7 vom: 01. Apr., Seite 765-76 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Gielis, Jan F [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 01.08.2011 Date Revised 13.12.2023 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.freeradbiomed.2010.12.018 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM20448636X |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM20448636X | ||
| 003 | DE-627 | ||
| 005 | 20231227124320.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231223s2011 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.freeradbiomed.2010.12.018 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1222.xml |
| 035 | |a (DE-627)NLM20448636X | ||
| 035 | |a (NLM)21172428 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Gielis, Jan F |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Pathogenetic role of eNOS uncoupling in cardiopulmonary disorders |
| 264 | 1 | |c 2011 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 01.08.2011 | ||
| 500 | |a Date Revised 13.12.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2010. Published by Elsevier Inc. | ||
| 520 | |a The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation. Chronically, eNOS has a major role in the regulation of blood pressure and prevention of atherosclerosis by decreasing leukocyte adhesion and smooth muscle proliferation. However, a disturbed vascular redox balance results in eNOS damage and uncoupling of oxygen activation from l-arginine conversion. Uncoupled eNOS monomerizes and generates reactive oxygen species (ROS) rather than NO. Indeed, eNOS uncoupling has been suggested as one of the main pathomechanisms in a broad range of cardiovascular and pulmonary disorders such as atherosclerosis, ventricular remodeling, and pulmonary hypertension. Therefore, modulating uncoupled eNOS, in particular eNOS-dependent ROS generation, is an attractive therapeutic approach to preventing and/or treating cardiopulmonary disorders, including protective effects during cardiothoracic surgery. This review provides a comprehensive overview of the pathogenetic role of uncoupled eNOS in both cardiovascular and pulmonary disorders. In addition, the related therapeutic possibilities such as supplementation with the eNOS substrate l-arginine, volatile NO, and direct NO donors as well as eNOS modulators such as the eNOS cofactor tetrahydrobiopterin and folic acid are discussed in detail | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Review | |
| 650 | 7 | |a Nitric Oxide Donors |2 NLM | |
| 650 | 7 | |a Reactive Oxygen Species |2 NLM | |
| 650 | 7 | |a Biopterins |2 NLM | |
| 650 | 7 | |a Nitric Oxide |2 NLM | |
| 650 | 7 | |a 31C4KY9ESH |2 NLM | |
| 650 | 7 | |a Folic Acid |2 NLM | |
| 650 | 7 | |a 935E97BOY8 |2 NLM | |
| 650 | 7 | |a Arginine |2 NLM | |
| 650 | 7 | |a 94ZLA3W45F |2 NLM | |
| 650 | 7 | |a NOS3 protein, human |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a Nitric Oxide Synthase Type III |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a sapropterin |2 NLM | |
| 650 | 7 | |a EGX657432I |2 NLM | |
| 650 | 7 | |a Oxygen |2 NLM | |
| 650 | 7 | |a S88TT14065 |2 NLM | |
| 700 | 1 | |a Lin, Judy Y |e verfasserin |4 aut | |
| 700 | 1 | |a Wingler, Kirstin |e verfasserin |4 aut | |
| 700 | 1 | |a Van Schil, Paul E Y |e verfasserin |4 aut | |
| 700 | 1 | |a Schmidt, Harald H |e verfasserin |4 aut | |
| 700 | 1 | |a Moens, An L |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Free radical biology & medicine |d 1989 |g 50(2011), 7 vom: 01. Apr., Seite 765-76 |w (DE-627)NLM012613827 |x 1873-4596 |7 nnns |
| 773 | 1 | 8 | |g volume:50 |g year:2011 |g number:7 |g day:01 |g month:04 |g pages:765-76 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.freeradbiomed.2010.12.018 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 50 |j 2011 |e 7 |b 01 |c 04 |h 765-76 | ||