Reactive Oxygen Species and Antioxidants in Pulmonary Hypertension

Wong, Chi‐Ming; Bansal, Geetanjali; Pavlickova, Ludmila; Marcocci, Lucia; Suzuki, Yuichiro

doi:10.1089/ars.2012.4568

Cited by 98 publications

(107 citation statements)

References 53 publications

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“…10 Finally, recent reports have linked disruption in the scavenging of reactive oxygen species to the progression and pathology of PH. 11,12 As an antioxidant, vitamin C may have multiple beneficial effects in scavenging reactive oxygen species and preventing downstream pulmonary vasoconstriction.…”

Section: Figurementioning

confidence: 99%

Pulmonary Hypertension Associated With Scurvy and Vitamin Deficiencies in an Autistic Child

Duvall¹,

Pikman

Kantor³

et al. 2013

Pediatrics

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Restricted dietary intake is common among children with behavioral issues. Here we report a case of a severely autistic child who presented initially with limp but who soon developed cough, tachypnea, hypoxia, and tachycardia. An echocardiogram revealed evidence of pulmonary hypertension (PH) with severely dilated right ventricle and elevated right-sided pressures. The etiology of his PH was unclear but further laboratory evaluation demonstrated severe nutritional deficiencies, in particular an undetectable ascorbic acid (vitamin C) level as well as deficient levels of thiamine (vitamin B 1 ), pyridoxine (vitamin B 6 ), cobalamin (vitamin B 12 ), and vitamin D. Repletion of these vitamins was associated with resolution of his PH and his musculoskeletal complaints. We report this case and a review of the relevant literature as a clinical lesson to expand the differential diagnosis of limp in children who may be difficult to assess as well as to report on an unusual association between severe vitamin deficiencies and PH.

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Section: Figurementioning

confidence: 99%

Pulmonary Hypertension Associated With Scurvy and Vitamin Deficiencies in an Autistic Child

Duvall¹,

Pikman

Kantor³

et al. 2013

Pediatrics

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“…An increased production of reactive oxygen species (ROS) may result from activated nicotinamide adenine dinucleotide phosphate reduced oxidases and dysfunctional mitochondria (48,49). ROS can oxidize tetrahydrobiopterin, an essential cofactor of eNOS, to dihydrobiopterin, which leads to eNOS uncoupling, a process by which eNOS produces superoxide instead of NO.…”

Section: Edno As a Paracrine Regulatormentioning

confidence: 99%

Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension

Gao

Chen

Raj

2016

Am J Respir Cell Mol Biol

119

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In the pulmonary vasculature, the endothelial and smooth muscle cells are two key cell types that play a major role in the pathobiology of pulmonary vascular disease and pulmonary hypertension. The normal interactions between these two cell types are important for the homeostasis of the pulmonary circulation, and any aberrant interaction between them may lead to various disease states including pulmonary vascular remodeling and pulmonary hypertension. It is well recognized that the endothelial cell can regulate the function of the underlying smooth muscle cell by releasing various bioactive agents such as nitric oxide and endothelin-1. In addition to such paracrine regulation, other mechanisms exist by which there is cross-talk between these two cell types, including communication via the myoendothelial injunctions and information transfer via extracellular vesicles. Emerging evidence suggests that these nonparacrine mechanisms play an important role in the regulation of pulmonary vascular tone and the determination of cell phenotype and that they are critically involved in the pathobiology of pulmonary hypertension.Keywords: paracrine; myoendothelial injunction; microvesicles; vasoconstriction; vascular remodelingIn the pulmonary vasculature, endothelial cells (ECs) and smooth muscle cells (SMCs) are the key cell types involved in the regulation of vessel diameter in most of the pulmonary vascular tree and thereby they regulate pulmonary arterial pressure and total vascular resistance. ECs, which are strategically located as the innermost layer of the blood vessel and are in contact with the circulating blood, exert a delicate and constant influence on the underlying vascular smooth muscle cells (VSMCs). It is well recognized that the regulation of pulmonary vasoreactivity by the endothelium is predominantly accomplished by paracrine signaling through the release of various vasoactive agents such as nitric oxide (NO), endothelin-1 (ET-1) (1-3), and others (4-8). However, there is increasing evidence that the relationship between the EC and the SMC is not a simple one-way interaction from the endothelium to the SMC; rather, there are complicated interactions between them (9-11). Moreover, the communication patterns are not limited to paracrine signaling; cross-talk through myoendothelial gap junctions (MEJs), extracellular vesicles (EVs), and other mechanisms is critically involved (12)(13)(14)(15)(16)(17)(18)(19)(20). These mechanisms operate in a complicated but co-ordinated manner to maintain the homeostasis of the pulmonary circulation. Under pathological conditions, the interaction between ECs and VSMCs may be chronically altered so that a sustained increase in vasocontractility and abnormal vascular proliferation develops, which leads to high pulmonary artery pressure, vascular remodeling, right ventricular hypertrophy, and the clinical condition, pulmonary hypertension (PH) (1,(21)(22)(23)(24). This article discusses the recent progress in our knowledge of the interactions between ECs and SMCs thr...

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“…[7][8][9] Accumulating data have shown that oxidative stress plays important roles in mediating pathological changes in the pulmonary arterioles and the right ventricle. [10][11][12] …”

Section: Reactive Oxygen Species (Ros)mentioning

confidence: 99%

Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension

2017

Chinese Medical Sciences Journal

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Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS), hypoxia inducible factors (HIF), and potassium channels (K V ) are believed as the main factors during the development of HPH. We propose that the "ROS/Kv/HIF axis" may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or K V , and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of "ROS/Kv/HIF axis" in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.

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Reactive Oxygen Species and Antioxidants in Pulmonary Hypertension

Cited by 98 publications

References 53 publications

Pulmonary Hypertension Associated With Scurvy and Vitamin Deficiencies in an Autistic Child

Pulmonary Hypertension Associated With Scurvy and Vitamin Deficiencies in an Autistic Child

Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension

Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension

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