SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation

Liu, Yue; Yang, Wenjian; Sun, Xiaodong; Xie, Lin; Yang, Yi; Sang, Ming; Jiao, Rong

doi:10.1007/s10753-019-01081-3

Cited by 46 publications

(19 citation statements)

References 32 publications

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“…Cardioprotective signaling pathways seems to converge on mitochondria especially to prevent inflammatory injury associated with CVD (Koenitzer and Freeman, 2010). Further, mitochondrion-targeted antioxidants show cardioprotective effects linked to reduction of NF-κB signaling and reduction of the expression of inflammatory cytokines (Liu et al, 2019). Supplementation with Coenzyme Q 10 plus selenium reduces the mortality by approximately 50% in patients with CVD in an effect associated to its bioenergetics, antioxidant and anti-inflammatory function (Mantle and Hargreaves, 2019).…”

Section: Cardiovascular Diseasementioning

confidence: 99%

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Fernández-Ayala

Navas

López-Lluch

2020

Experimental Gerontology

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SARS-CoV-2 causes a severe pneumonia (COVID-19) that affects essentially elderly people. In COVID-19, macrophage infiltration into the lung causes a rapid and intense cytokine storm leading finally to a multi-organ failure and death. Comorbidities such as metabolic syndrome, obesity, type 2 diabetes, lung and cardiovascular diseases, all of them age-associated diseases, increase the severity and lethality of COVID-19. Mitochondrial dysfunction is one of the hallmarks of aging and COVID-19 risk factors. Dysfunctional mitochondria is associated with defective immunological response to viral infections and chronic inflammation. This review discuss how mitochondrial dysfunction is associated with defective immune response in aging and different age-related diseases, and with many of the comorbidities associated with poor prognosis in the progression of COVID-19. We suggest here that chronic inflammation caused by mitochondrial dysfunction is responsible of the explosive release of inflammatory cytokines causing severe pneumonia, multi-organ failure and finally death in COVID-19 patients. Preventive treatments based on therapies improving mitochondrial turnover, dynamics and activity would be essential to protect against COVID-19 severity.

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Section: Cardiovascular Diseasementioning

confidence: 99%

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Fernández-Ayala

Navas

López-Lluch

2020

Experimental Gerontology

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“…inflammatory responses in heart tissues and cultured CFs. Although the molecular mechanisms of SIC remain to be fully elucidated, inflammatory responses are acknowledged as a main contributor to the occurrence and development of SIC (32,33). In this study, LPS acted as a vital contributor to NF-κB activation, which can lead to the transcription of proinflammatory cytokines such as IL-6, IL-1β and TNF-α (34).…”

Section: Il-35 Pretreatment Attenuates Lps-induced Heart Injurymentioning

confidence: 87%

Interleukin-35 pretreatment attenuates lipopolysaccharide-induced heart injury by inhibition of inflammation, apoptosis and fibrosis

et al. 2020

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Previous studies have demonstrated that targeting inflammation is a promising strategy for treating lipopolysaccharide (LPS)-induced sepsis and related heart injury. Interleukin-35 (IL-35), which consists of two subunits, Epstein-Barr virus-induced gene 3 (EBI3) and p35, is an immunosuppressive cytokine of the IL-12 family and exhibits strong anti-inflammatory activity. However, the role of IL-35 in LPS-induced heart injury remains obscure. In this study, we explored the role of IL-35 in heart injury induced by LPS and its potential mechanisms. Mice were treated with a plasmid encoding IL-35 (pIL-35) and then injected intraperitoneally (ip) with LPS (10 mg/kg). Cardiac function was assessed by echocardiography 12 h later. LPS apparently decreased the expression of EBI3 and p35 and caused cardiac dysfunction and pathological changes, which were significantly improved by

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“…Antioxidants are beneficial in COPD as they inhibit the inflammatory response [30]. SS-31 was shown to suppress inflammation, as evidenced by the decreased levels of IL-6, IL-1β [16,31], TNF-α [31], and MMP9 [14]. Additionally, SS-31 restored the activities of SOD, MDA [30], and MPA .…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial‐Targeting Antioxidant SS‐31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke

Yang

Zuo

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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This study investigated whether the mitochondrial-targeted peptide SS-31 can protect against cigarette smoke- (CS-) induced airway inflammation and oxidative stress in vitro and in vivo. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure. Pathologic changes and oxidative stress in lung tissue, inflammatory cell counts, and proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were examined. The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues. SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF. SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD). It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol. Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression. RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo. Thus, SS-31 alleviates CS-induced airway inflammation and oxidative stress via modulation of mitochondrial function and regulation of MAPK signaling and thus has therapeutic potential for the treatment of airway disorders caused by smoking.

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SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation

Cited by 46 publications

References 32 publications

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Interleukin-35 pretreatment attenuates lipopolysaccharide-induced heart injury by inhibition of inflammation, apoptosis and fibrosis

Mitochondrial‐Targeting Antioxidant SS‐31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke

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