Nitro-Fatty Acids: Formation, Redox Signaling, and Therapeutic Potential

Trostchansky, Andrés; Bonilla, Lucía; González-Perilli, Lucía; Rubbo, Homero

doi:10.1089/ars.2012.5023

Cited by 51 publications

(29 citation statements)

References 72 publications

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“…NO-derived species (reactive nitrogen species, RNS), such as •NO 2 , ONOO − , HNO 2 , and NO 2 + , can oxidize or nitrate PUFAs and yield nitrated fatty acids (NO 2 -FA) (Figure 2). NO 2 -FA is an electrophile, which readily reacts with nucleophilic amino acids such as histidine and cysteine and changes protein function and catalytic activity [46, 47]. Importantly, NO 2 -FA appears to target specific proteins [48].…”

Section: Mode Of Action Of Nitric Oxidementioning

confidence: 99%

Nitric oxide in liver diseases

Iwakiri

Kim

2015

Trends in Pharmacological Sciences

224

183

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Nitric oxide (NO) and its derivatives play important roles in the physiology and pathophysiology of the liver. Despite its diverse and complicated roles, certain patterns of the effect of NO on the pathogenesis and progression of liver diseases are observed. In general, NO derived from endothelial NO synthase (eNOS) in liver sinusoidal endothelial cells (LSECs) is protective against disease development, while inducible NOS (iNOS)-derived NO contributes to pathological processes. This review addresses the roles of NO in the development of various liver diseases with a focus on recently published articles. We present here two recent advances in understanding NO-mediated signaling, nitrated fatty acids and S-guanylation, and conclude with suggestions on future directions of NO-related studies on the liver.

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Section: Mode Of Action Of Nitric Oxidementioning

confidence: 99%

Nitric oxide in liver diseases

Iwakiri

Kim

2015

Trends in Pharmacological Sciences

224

183

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“…Regulatory functions for the cardiovascular system have also been demonstrated for nitrated fatty acids [75]. These electrophilic compounds can be generated in the reaction of unsaturated fatty acids with NO-derived reactive species and act via NO-dependent and NO-independent pathways [76].…”

Section: No-generating Agentsmentioning

confidence: 99%

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Blecharz-Lang¹,

Burek²

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Imbalances in the synthesis or in the bioavailability of nitric oxide (NO), the freely diffusible vasodilator, in myocardial endothelial cells were demonstrated to be crucial in the development of hypertension. Glucocorticoids (GCs) are widely used as immunomodulators. One of the numerous side effects of GC therapy is hypertension arising from reduced release of the endothelium-derived NO. GCs can modulate NO synthesis by targeting the genes involved in it, like nitric oxide synthase (NOS) and guanosine triphosphate (GTP) cyclohydrolase-1 (GTPCH-1). This chapter will give an overview on the impact of GCs on NO synthesis and signalling in animal models as well as in in vitro cell culture models. Moreover, strategies for preventing or neutralizing side effects of long-term GC therapy will be discussed.

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“…NO 2 -FAs release NO and possess antioxidant functions [244]. Therefore, NO 2 -FAs may be promising pharmacological tools as NO donors to prevent inflammatory diseases associated with redox imbalance [245]. In addition, NO 2 -FAs may function independently of NO.…”

Section: Therapeutic Strategies For Redox Regulation Of Ec Fatementioning

confidence: 99%

Redox regulation of endothelial cell fate

Song

2014

Cell. Mol. Life Sci.

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Endothelial cells (ECs) are present throughout blood vessels and have variable roles in both physiological and pathological settings. EC fate is altered and regulated by several key factors in physiological or pathological conditions. Reactive nitrogen species and reactive oxygen species derived from NAD(P)H oxidases, mitochondria, or nitric oxide-producing enzymes are not only cytotoxic but also compose a signaling network in the redox system. The formation, actions, key molecular interactions, and physiological and pathological relevance of redox signals in ECs remain unclear. We review the identities, sources, and biological actions of oxidants and reductants produced during EC function or dysfunction. Further, we discuss how ECs shape key redox sensors and examine the biological functions, transcriptional responses, and post-translational modifications evoked by the redox system in ECs. We summarize recent findings regarding the mechanisms by which redox signals regulate the fate of ECs and address the outcome of altered EC fate in health and disease. Future studies will examine if the redox biology of ECs can be targeted in pathophysiological conditions.

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Nitro-Fatty Acids: Formation, Redox Signaling, and Therapeutic Potential

Cited by 51 publications

References 72 publications

Nitric oxide in liver diseases

Nitric oxide in liver diseases

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data

Redox regulation of endothelial cell fate

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