The complex role of iNOS in acutely rejecting cardiac transplants

Pieper, Galen M.; Roza, Allan M.

doi:10.1016/j.freeradbiomed.2008.01.020

Cited by 18 publications

(7 citation statements)

References 146 publications

(195 reference statements)

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“…Similar effects were seen when using so called NO neutralizers [48,49]. An extensive review on the role of iNOS in acutely cardiac transplant rejection is given by Pieper and Roza [50].…”

Section: Heartmentioning

confidence: 72%

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Mehl¹,

Grasemann²

2010

TONOJ

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Since the discovery of nitric oxide (NO) in biological systems more than 20 years ago, it became widely accepted that endogenous NO plays a key role in the regulation of a variety of physiological processes. NO is involved in reperfusion injury and chronic rejection after solid organ transplantation. Arginase is an enzyme that competes with NO synthases for the common substrate L-arginine. Increased arginase activity alters L-arginine metabolism and reduces substrate availability for NO synthases, and thereby contributes to organ dysfunction following transplantation. NO deficiency after lung transplantation impacts on perfusion and ventilation of the donor organ. L-ornithine, the product of arginase activity, is precursor for polyamine and proline biosynthesis which are both involved in airway remodeling. The purpose of this review is to summarize the current knowledge on the role of alterations in the L-arginine metabolism in lung transplantation.

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“…Similar effects were seen when using so called NO neutralizers [48,49]. An extensive review on the role of iNOS in acutely cardiac transplant rejection is given by Pieper and Roza [50].…”

Section: Heartmentioning

confidence: 72%

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Mehl¹,

Grasemann²

2010

TONOJ

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“…Blockade of NO production by iNOS inhibitors has been shown to prolong skin xenograft survival by down-regulation of the expressions of proinflammatory cytokines [41]. On the other hand, it is reported that NO derived from iNOS has a dual role in cardiac transplantation: detrimental in acute rejection and beneficial in chronic rejection [42]. Causal relationships between platonin-induced iNOS inhibition and attenuated skin graft rejection deserve further investigation.…”

Section: Discussionmentioning

confidence: 99%

Platonin Improves Survival of Skin Allografts

Cheng

Lee

Chi

et al. 2010

Journal of Surgical Research

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“…Administration of an NO donor reverses these adverse effects on yolk sac vasculature 22 . Additionally, it has been reported that NO derived from iNOS plays a detrimental role in human disease 101 . Moreover, iNOS and eNOS are expressed during early embryonic vasculogenesis, and the alteration of NO expression induces yolk sac vasculopathy 22 .…”

Section: Molecular Intermediates and Signaling Pathways Contribute Tomentioning

confidence: 99%

New development of the yolk sac theory in diabetic embryopathy: molecular mechanism and link to structural birth defects

Dong

Reece

Xue

et al. 2016

American Journal of Obstetrics and Gynecology

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Maternal diabetes is a significant risk factor for structural birth defects, including congenital heart defects and neural tube defects (NTDs). With the rising prevalence of type 2 diabetes and obesity in women of childbearing age, diabetes-induced birth defects have become an increasingly significant public health problem. Maternal diabetes in vivo and high glucose in vitro induce yolk sac injuries by damaging the morphology of cells and altering the dynamics of organelles. The yolk sac vascular system is the first system to develop during embryogenesis, therefore, it is the most sensitive to hyperglycemia. The consequences of yolk sac injuries include impairment of nutrient transportation due to vasculopathy. Although the functional relationship between yolk sac vasculopathy and structural birth defects has not yet been established, a recent study reveals that the quality of yolk sac vasculature is inversely related to embryonic malformation rates. Studies in animal models have uncovered key molecular intermediates of diabetic yolk sac vasculopathy, including hypoxia-inducible factor-1α (HIF-1α), apoptosis signal-regulating kinase 1 (ASK1) and its inhibitor thioredoxin-1 (Trx), c-Jun-N-terminal kinases (JNK), nitric oxide (NO) and nitric oxide synthase (NOS). Yolk sac vasculopathy is also associated with abnormalities in arachidonic acid and myo-inositol. Dietary supplementation with fatty acids that restore lipid levels in the yolk sac lead to reduction in diabetes-induced malformations. Although the role of the human yolk in embryogenesis is less extensive than in rodents, nevertheless, human embryonic vasculogenesis is negatively affected by maternal diabetes. Mechanistic studies have identified potential therapeutic targets for future intervention against yolk sac vasculopathy, birth defects, and other complications associated with diabetic pregnancies.

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The complex role of iNOS in acutely rejecting cardiac transplants

Cited by 18 publications

References 146 publications

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Alterations in L-Arginine Metabolism After Lung Transplantation~!2009-11-12~!2010-03-25~!2010-05-04~!

Platonin Improves Survival of Skin Allografts

New development of the yolk sac theory in diabetic embryopathy: molecular mechanism and link to structural birth defects

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