Endothelial Nitric Oxide Synthase in Vascular Disease: From Marvel to Menace

By U. Förstermann, T. Münzel. Circulation, 2006

1,928 citations recorded by the source corpus.

Subfields: Biochemistry, Cardiology and Cardiovascular Medicine, Physiology

View Paper: https://www.semanticscholar.org/paper/3e8937bb932fd4671e40ad7d4130166880c3544e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biochemistry

1. U. Förstermann
2. Huige Li
3. Sven Horke
4. D. Granger
5. P. Kvietys

In Cardiology and Cardiovascular Medicine

1. U. Förstermann
2. Huige Li
3. D. Granger
4. P. Kvietys
5. Sven Horke

In Physiology

1. U. Förstermann
2. Huige Li
3. Sven Horke
4. D. Granger
5. P. Kvietys

Citations in the corpus

• Vascular oxidative stress, nitric oxide and atherosclerosis. (2014, background): “Peroxynitrite, the direct reaction product of NO and superoxide, is capable of oxidizing BH4 and thus leading to BH 4 deficiency [5, 64].”
• Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease (2019, background): “In short, there is an indispensable role played by oxidative stress in the development of cardiovascular disease, both mediated somewhat by the uncoupling of endothelial nitric oxide synthase (eNOS) [77], making eNOS uncoupling a hallmark of most cardiovascular diseases [110, 111].”
• Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, neutral): “NO, a condition called “eNOS uncoupling” [136].”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “Of these isoforms, only eNOS is the membrane-associated protein and is the predominant source of NO in vascular endothelial cells (121).”
• Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “The monomer in isolation cannot couple O2 reduction to NO synthesis and generates O2 ·− instead [395,396].”
• Endothelial Dysfunction in Atherosclerotic Cardiovascular Diseases and Beyond: From Mechanism to Pharmacotherapies (2021, background): “In healthy endothelial cells, NO is produced from L-arginine via endothelial nitric oxide synthase (eNOS), with help from tetrahydrobiopterin (BH4) as a cofactor (Förstermann and Münzel, 2006).”