Role of Mitochondria in the Redox Signaling Network and Its Outcomes in High Impact Inflammatory Syndromes

Magnani, Natalia; Marchini, Timoteo; Calabró, Valeria; Álvarez, Silvia; Evelson, Pablo

doi:10.3389/fendo.2020.568305

Cited by 35 publications

(29 citation statements)

References 196 publications

(264 reference statements)

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“…These molecules bind to vascular endothelial adhesion molecules, such as ICAM-1 and VCAM-1, facilitating the transmigration of leukocytes through the activated endothelium to the site of injury [ 19 ]. The utility of chemokines lies in recruiting additional immune cells and proteins such as iNOS that generate nitric oxide (NO) [ 20 ]. Instead, NLRs are involved in the formation of multiple protein signaling complexes known as inflammasomes.…”

Section: Inflammationmentioning

confidence: 99%

Contribution of oxidative stress in the mechanisms of postoperative complications and multiple organ dysfunction syndrome

Perez

Rodrigo

2021

Redox Report

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Background The extent of the damage following surgery has been subject of study for several years. Numerous surgical complications can impact postoperative quality of life of patients and even can cause mortality. Although these complications are generally due to multifactorial mechanisms, oxidative stress plays a key pathophysiological role. Moreover, oxidative stress could be an unavoidable effect derived even from the surgical procedure itself. Methods A systematic review was performed following an electronic search of Pubmed and ScienceDirect databases. Keywords such as sepsis, oxidative stress, organ dysfunction, antioxidants, outcomes in postoperative complications, among others, were used. Review articles were preferably used between the years 2015 onwards, not excluding older ones. Results The vast majority point to the role of oxidative stress in generating greater damage and worse prognosis in postoperative patients without the necessary care and precautions, taking importance on the use of antioxidants to prevent this problem. Discussions Oxidative stress represents a common final pathway related to pathological processes such as inflammation or ischemia–reperfusion, among others. The expression of greater severity of these complications can result in multiple organ dysfunction or sepsis. The aim of this study was to present an update of the role of oxidative stress on surgical postoperative complications.

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Section: Inflammationmentioning

confidence: 99%

Contribution of oxidative stress in the mechanisms of postoperative complications and multiple organ dysfunction syndrome

Perez

Rodrigo

2021

Redox Report

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“…After LPS induction, the production of ROS in BV-2 cells increased. Then, the overladen ROS caused membrane phospholipid to be attacked by free radical ( Magnani et al, 2020 ), leading to the loss of MMP and, in turn, mitochondrial dysfunction and ATP depletion. It was outstanding that ACT treatment mitigated the decrease of MMP and ATP content.…”

Section: Discussionmentioning

confidence: 99%

An Inhibitor of NF-κB and an Agonist of AMPK: Network Prediction and Multi-Omics Integration to Derive Signaling Pathways for Acteoside Against Alzheimer’s Disease

Chen

Jiang

et al. 2021

Front. Cell Dev. Biol.

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Alzheimer’s disease (AD) is the most frequent type of dementia. Acteoside (ACT) is a compound isolated from Cistanche tubulosa, which possesses excellent neuroprotective properties. However, the underlying mechanism of ACT in regulating microglia polarization remains ill-defined. Therefore, a computational network model was established to identify the driving targets of ACT and predict its mechanism by integrating multiple available databases. The AlCl3-induced AD model in zebrafish larvae was successfully constituted to demonstrate the therapeutic efficacy of ACT. Subsequently, LPS-induced BV-2 cells uncovered the positive role of ACT in M1/M2 polarization. The NF-κB and AMPK pathways were further confirmed by transcriptomic analysis, metabolomics analysis, molecular biology techniques, and molecular docking. The research provided an infusive mechanism of ACT and revealed the connection between metabolism and microglia polarization from the perspective of mitochondrial function. More importantly, it provided a systematic and comprehensive approach for the discovery of drug targets, including the changes in genes, metabolites, and proteins.

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“…After induced by LPS, the production of ROS increased in BV-2 cells. Then the overladen ROS caused membrane phospholipid to be attacked by free radical [25] . It led to the loss of MMP, in turn mitochondrial dysfunction and ATP depletion.…”

Section: Discussionmentioning

confidence: 99%

Acteoside Repressed Microglia M1 Polarization Through Inhibited NF-κB Signalling Pathway and AMPK-Mediated Mitochondria Function Recovery

Chen

Jiang

et al. 2020

Preprint

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Background: Alzheimer's disease (AD) is the most frequent type of dementia. While acteoside (ACT), a compound isolated from Cistanche tubulosa, possesses neuroprotective properties. However, the underlying mechanism in regulating microglia polarization remains ill-defined. Methods: Herein, AlCl3-induced AD model in zebrafish larvae was applied to uncover the therapeutic efficacy of ACT. BV-2 cells were used to demonstrate the role of ACT on microglia polarization. RNA-Sequence, HPLC-Q-TOF-MS, western blot and molecular docking were combined to confirm its mechanism. Results: ACT significantly ameliorated the experimental dyskinesia and nervous system disorders in zebrafish. Subsequently, it suppressed M1 polarization and promoted to the M2 phenotype in LPS-induced BV-2 cells. We first demonstrated that ACT exerted profound transcriptomic impact, which involved regulation of key signaling pathways in inflammation, arginine biosynthesis, as well as pantothenate and CoA biosynthesis, correlating with mitochondria function. ACT treatment reduced microglia M1 polarization by inhibiting the NF-κB signalling pathway. And the metabolic pathways were further confirmed by HPLC-Q-TOF-MS. In addition, ACT rectified excessive ROS to restore mitochondria function through AMPK-mediated PGC-1α and UCP-2 upregulation, consistent with metabolic changes. Intriguingly, ACT may directly bind to both NF-κB and AMPKα, as evidenced by molecular docking. Conclusions: The research provided an infusive mechanism of ACT and illustrated a new perspective based on mitochondrial dysfunction to reveal the connection between metabolism and microglia polarization.

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Role of Mitochondria in the Redox Signaling Network and Its Outcomes in High Impact Inflammatory Syndromes

Cited by 35 publications

References 196 publications

Contribution of oxidative stress in the mechanisms of postoperative complications and multiple organ dysfunction syndrome

Contribution of oxidative stress in the mechanisms of postoperative complications and multiple organ dysfunction syndrome

An Inhibitor of NF-κB and an Agonist of AMPK: Network Prediction and Multi-Omics Integration to Derive Signaling Pathways for Acteoside Against Alzheimer’s Disease

Acteoside Repressed Microglia M1 Polarization Through Inhibited NF-κB Signalling Pathway and AMPK-Mediated Mitochondria Function Recovery

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