Kidney failure, arterial hypertension and left ventricular hypertrophy in rats with loss of function mutation of SOD3

Guo, Haipeng; Xu, Dan; Kuroki, Marcos T.; Lu, Zhigang; Xu, Xin; Geurts, Aron M.; Osborn, John W.; Chen, Yingjie

doi:10.1016/j.freeradbiomed.2020.01.023

Cited by 18 publications

(15 citation statements)

References 39 publications

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“…Specifically, global EcSOD knockout mice (EcSOD -/-) showed similar blood pressure at baseline compared with the wild type littermates, but displayed exacerbated hypertension following angiotensin II administration (41). A novel rat strain with loss-offunction mutation of EcSOD E124D in the Dahl/Salt Sensitive (Dahl/SS) background developed age-dependent arterial hypertension along with kidney failure and cardiac hypertrophy (45).…”

Section: Catabolic Muscle Wastingmentioning

confidence: 99%

“…Acute kidney injury (AKI). Mouse models in which the EcSOD gene is mutated or SOD inhibitors are used suggest protective role of EcSOD against renal injury (19,45,95,104).…”

Section: Copdmentioning

confidence: 99%

“…When EcSOD was mutated at amino acid 124 from glutamic acid to aspartic acid (EcSOD E124D ) in rats, spontaneous CKD occurred in an age-dependent manner as a result of increased renal oxidative stress, inflammation, and fibrosis (45). Additional animal studies provided more definitive evidence for the protective role of EcSOD against CKD.…”

Section: Copdmentioning

confidence: 99%

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Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise

2020

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Extracellular superoxide dismutase (EcSOD) is the only extracellular scavenger of superoxide anion (O 2 .-) with unique binding capacity to cell surface and extracellular matrix through its heparin-binding domain. Enhanced EcSOD activity prevents oxidative stress and damage, which are fundamental in a variety of disease pathologies. In this review we will discuss the findings in humans and animal studies supporting the benefits of EcSOD induced by exercise training in reducing oxidative stress in various tissues. In particularly, we will highlight the importance of skeletal muscle EcSOD, which is induced by endurance exercise and redistributed through the circulation to the peripheral tissues, as a molecular transducer of exercise training to confer protection against oxidative stress and damage in various disease conditions.

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Section: Catabolic Muscle Wastingmentioning

confidence: 99%

“…Acute kidney injury (AKI). Mouse models in which the EcSOD gene is mutated or SOD inhibitors are used suggest protective role of EcSOD against renal injury (19,45,95,104).…”

Section: Copdmentioning

confidence: 99%

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Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise

2020

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“…We previously reported that antioxidant reagents, such as EUK-8, MnTBAP, manganese porphyrins, and apple procyanidins, improved DCM accompanied by a reduction in mitochondrial ROS accumulation in Sod2 H/H mice [23,[60][61][62]. Recently, Guo et al reported that a loss-of-function mutation in extracellular SOD (SOD3) induced chronic kidney disease accompanied by systolic hypertension and cardiac hypertrophy in a Dahl/salt-sensitive strain of rats [63]. In addition, SOD3 KO mice also showed hypoxia-induced pulmonary vascular disease [64,65].…”

Section: Discussionmentioning

confidence: 99%

Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice

Watanabe

Shibuya

Ozawa

et al. 2021

IJMS

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Intracellular superoxide dismutases (SODs) maintain tissue homeostasis via superoxide metabolism. We previously reported that intracellular reactive oxygen species (ROS), including superoxide accumulation caused by cytoplasmic SOD (SOD1) or mitochondrial SOD (SOD2) insufficiency, induced p53 activation in cells. SOD1 loss also induced several age-related pathological changes associated with increased oxidative molecules in mice. To evaluate the contribution of p53 activation for SOD1 knockout (KO) (Sod1−/−) mice, we generated SOD1 and p53 KO (double-knockout (DKO)) mice. DKO fibroblasts showed increased cell viability with decreased apoptosis compared with Sod1−/− fibroblasts. In vivo experiments revealed that p53 insufficiency was not a great contributor to aging-like tissue changes but accelerated tumorigenesis in Sod1−/− mice. Furthermore, p53 loss failed to improve dilated cardiomyopathy or the survival in heart-specific SOD2 conditional KO mice. These data indicated that p53 regulated ROS-mediated apoptotic cell death and tumorigenesis but not ROS-mediated tissue degeneration in SOD-deficient models.

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“…Red blood cells of Sod1 knockout mice present high ROS levels (and oxidative stress) and show evidence of an autoimmune response (Iuchi et al., 2007), emphasizing the role of SOD1 in maintaining an appropriate redox balance. SOD2 has been implicated in mitochondrial dysfunction and neurodegenerative disorders (Flynn & Melov, 2013), whereas SOD3 dysregulation is associated with pulmonary, cardiovascular and neoplastic pathologies (Guo et al., 2020; Kwon et al., 2015; Pereira et al., 2019). As outlined above, higher SOD activity has been observed in diving species; however, little is known about the evolution of the SOD gene family in diving mammals (Miller, 2012).…”

Section: Introductionmentioning

confidence: 99%

Comparative analysis of the superoxide dismutase gene family in Cetartiodactyla

Tian

Geng

Guo

et al. 2021

J of Evolutionary Biology

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Cetacea, whales, dolphins and porpoises form an order of mammals adapted to aquatic life. Their transition to an aquatic habitat resulted in exceptional protection against cellular insults, including oxidative and osmotic stress. Here, we considered the structure and molecular evolution of the superoxide dismutase (SOD) gene family, which encodes essential enzymes in the mammalian antioxidant system, in the superorder Cetartiodactyla. To this end, we juxtaposed cetaceans and their closest extant relatives (order Artiodactyla). We identified 94 genes in 23 species, of which 70 are bona fide intact genes. Although the SOD gene family is conserved in Cetartiodactyla, lineage‐specific gene duplications and deletions were observed. Phylogenetic analyses show that the SOD2 subfamily diverged from a clade containing SOD1 and SOD3, suggesting that cytoplasmic, extracellular and mitochondrial SODs have started down independent evolutionary paths. Specific‐amino acid changes (e.g. K130N in SOD2) that may enhance ROS elimination were identified in cetaceans. In silico analysis suggests that the core transcription factor repertoire of cetartiodactyl SOD genes may include Sp1, NF‐κB, Nrf2 and AHR. Putative transcription factors binding sites responding to hypoxia were (e.g. Suppressor of Hairless; Su(H)) found in the cetacean SOD1 gene. We found significant evidence for positive selection in cetaceans using codon models. Cetaceans with different diving abilities also show divergent evolution of SOD1 and SOD2. Our genome‐wide analysis of SOD genes helps clarify their relationship and evolutionary trajectory and identify putative functional changes in cetaceans.

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Kidney failure, arterial hypertension and left ventricular hypertrophy in rats with loss of function mutation of SOD3

Cited by 18 publications

References 39 publications

Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise

Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise

Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice

Comparative analysis of the superoxide dismutase gene family in Cetartiodactyla

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