Mitochondria-Targeted Antioxidant Mito-Tempo Protects Against Aldosterone-Induced Renal Injury In Vivo

Ding, Wei; Liu, Tingyan; Bi, Xiao; Zhang, Zhiling

doi:10.1159/000485287

Cited by 32 publications

(22 citation statements)

References 32 publications

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“…Furthermore, it has been shown that NLRP3 can directly promote the TGF-β signal and activation of R-Smad independent of inflammasome (Wang et al, 2013), which offers new insights into the function and potential treatments of NLRP3 inflammasome in kidney disease. In addition, there are other potential treatment or drugs can reduce or inhibit tubular damage by interfering with the signal pathway of NLRP3 inflammasome; these include mitochondria target antioxidants, compound K, Neferine, allopurinol, and ghrelin (Ding et al, 2017;Foresto-Neto et al, 2018;Hsu et al, 2019;Ling et al, 2019).…”

Section: Inflammasomes In Chronic Kidney Diseasementioning

confidence: 99%

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Xiang

Zhu

et al. 2020

Front. Cell Dev. Biol.

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Inflammasomes, multiprotein complex induced by harmful factors in the body, play a crucial role in innate immunity. Activation of inflammasomes lead to the activation of casepase-1 and then the secretion of inflammatory cytokines, including IL-1β and IL-18, subsequently leading to a type of cell death called pyroptosis. There are two types of signaling pathways involved in the process of inflammasome activation: the canonical and the non-canonical signaling pathway. The canonical signaling pathway is mainly dependent on casepase-1; the non-canonical signal pathway, which was recently discovered, is mainly dependent on caspase-11, but is also meditated by caspase-4, caspase-5, and caspase-8. Kidney inflammation is basically associated with inflammatory factor exudation and inflammatory cell infiltration. Several studies have showed that inflammasomes are closely related to kidney diseases, especially the NOD-, LRR-and pyrin domain-containing 3 (NLRP3) inflammasome, which play a role in regulating kidney inflammation and fibrosis. In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways.

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Section: Inflammasomes In Chronic Kidney Diseasementioning

confidence: 99%

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Xiang

Zhu

et al. 2020

Front. Cell Dev. Biol.

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“…ROS could be generated from different sources including mitochondria, ER stress, lysosomal dysfunction, and oxidases . Various ROS scavengers could inhibit ROS production through different manners as briefly shown in the figure .…”

Section: Treatment Of Antioxidants For Suppressing Nlrp3 Inflammasomementioning

confidence: 99%

Role and mechanism of ROS scavengers in alleviating NLRP3‐mediated inflammation

Sho

2018

Biotech and App Biochem

101

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Inflammation, as a common immune response to various infections or injuries, can cause many dangerous and complicated diseases. Inflammasome is a protein complex playing a vital role in an inflammation process, and the nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome has been the most-widely studied one. Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model. Numerous recent preclinical reports indicate that application of antioxidants could scavenge excessive ROS and attenuate inflammatory responses through suppressing NLRP3 inflammasome activation. This article, at first, briefly overviews how ROS may mediate the regulation of NLRP3 inflammasome activation. Then, preclinical researches of various ROS scavengers for treating NLRP3 inflammasome-associated diseases are focused on and critically analyzed. Finally, the potential of antioxidant treatment as a therapy for inflammation is to be discussed, and perspectives on future research directions will be shared.

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“…It has been reported that mito‐T is a potent mitochondria‐targeted antioxidant, which could act in ischemic tissues linked with hypoxia‐induced oxidative stress (Ding, Liu, Bi, & Zhang, 2017; Du et al, 2019; Du, Farhood, & Jaeschke, 2017; Li et al, 2018; Liu, Wang, Ding, & Wang, 2018; Nautiyal, Shaltout, Chappell, & Diz, 2019; Shetty, Kumar, & Bharati, 2019; Yang et al, 2018; Zhan et al, 2018). In the present study, mito‐T, a mitochondria‐targeted superoxide dismutase mimetic, dramatically reduced AMA‐induced mitochondrial oxidative stress, and thus effectively protected MSCs.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that mito-T is a potent mitochondriatargeted antioxidant, which could act in ischemic tissues linked with hypoxia-induced oxidative stress (Ding, Liu, Bi, & Zhang, 2017;Du et al, 2019;Du, Farhood, & Jaeschke, 2017;Li et al, 2018;Liu, Wang, Ding, & Wang, 2018;Nautiyal, Shaltout, Chappell, & Diz, 2019;Shetty, Kumar, & Bharati, 2019;Yang et al, 2018;Zhan et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Mitochondria‐targeted antioxidant mito‐TEMPO alleviate oxidative stress induced by antimycin A in human mesenchymal stem cells

Nouri

Gueguen

Saeedi

et al. 2020

Journal Cellular Physiology

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The cell therapy of damaged tissue, which is linked to hypoxia condition might fail, in large part due to the emergence of oxidative stress (OS) and/or mitochondrial dysfunctions. Thus, the invigoration of stem cells against oxidative stress could be a reliable strategy to improve the cell therapy outcome. Of various antioxidants, mito‐Tempo (mito‐T) is one of the potent antioxidants that could target and neutralize the mitochondrial oxidative stress. In this study, for the induction of hypoxia and oxidative stress in mitochondria of the mesenchymal stem cells (MSCs) isolated from human adipose tissue, antimycin A (AMA) was used and then several parameters were analyzed, including cell viability and cell cycle arrest of MSCs exposed to AMA, mito‐T, antioxidant potential, redox homeostasis, and signaling pathways in MSCs under oxidative stress. Based on our findings, the treated MSCs were found to impose a high resistance to the OS‐induced apoptosis, which correlated with the nuclear factor erythroid 2‐related factor 2 (Nrf2) pathway required to manage OS. Upon exposure of the MSCs to high oxidative stress conditions using AMA, the cells failed to scavenge. The use of mito‐T was found to alleviate the damage induced by oxidative stress through both direct functions of the free radical scavenging and the interplay in terms of cell signaling pathways including the upregulation of the Nrf2 pathway. These findings may pave the way in the stem cell therapy for the hypoxia‐mediated tissue damage.

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Mitochondria-Targeted Antioxidant Mito-Tempo Protects Against Aldosterone-Induced Renal Injury In Vivo

Cited by 32 publications

References 32 publications

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Role and mechanism of ROS scavengers in alleviating NLRP3‐mediated inflammation

Mitochondria‐targeted antioxidant mito‐TEMPO alleviate oxidative stress induced by antimycin A in human mesenchymal stem cells

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