Juglanin alleviates bleomycin-induced lung injury by suppressing inflammation and fibrosis via targeting sting signaling

Sun, Jie; Han, Ru; Hou, Shuangshuang; Yi, Huanfa; Shou-jun, Chi; Zhang, Aihua

doi:10.1016/j.biopha.2020.110119

Cited by 33 publications

(20 citation statements)

References 36 publications

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“…41 STING also contributes to bleomycininduced idiopathic pulmonary fibrosis and lung injury, which could be alleviated by juglanin. 42 Additionally, acute exposure to cigarette smoke also causes airway inflammation with fibrosis and emphysema of mice in a STING-dependent manner. 43 Our recent study proposed that STING may drive NLRP3 inflammasome-mediated pyroptosis and cellular injury in sepsis-induced cardiac injury.…”

Section: Discussionmentioning

confidence: 99%

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Wang

Jiang

et al. 2020

Clinical & Translational Med

173

125

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Section: Discussionmentioning

confidence: 99%

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Wang

Jiang

et al. 2020

Clinical & Translational Med

173

125

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“…Juglanin 132 , a natural constituent mainly extracted from Juglans mandshurica Maxim., could protect against LPS-triggered ALI in vivo and in vitro via inhibition of fibrosis markers (TGF-β1, α-SMA, collagen type III and collagen type I) and inflammatory cytokine production (TNF-α, IL-1β, IL-18, IL-6, IL-4 and IL-17) through blocking the NF-κB signaling pathway [ 372 ]. Due to its anti-inflammatory and anti-fibrosis activities, juglanin could also prevent bleomycin-induced lung injury, which is related to inhibition of the Sting signaling pathway [ 373 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

248

121

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“…Different publications using genetically modified animals confirmed the role of STING in models of lung inflammation [ 27 , 28 , 29 ]. Although therapeutic intervention in the cGAS/STING pathway might lead to some improvements in diseases such as cirrhosis and endomyocardial fibrosis [ 30 , 31 , 32 , 33 , 34 , 35 ], more data would be needed to confirm a strong general effect in fibrosis. Aberrant cGAS/STING activation might also play a role in diseases such as nonalcoholic steatohepatitis (NASH) and chronic obstructive pulmonary disease (COPD); nevertheless, this still requires further evaluation.…”

Section: The Cgas/sting a Nucleic Acid Sensing Pathway Plays A Role I...mentioning

confidence: 99%

STING Agonists/Antagonists: Their Potential as Therapeutics and Future Developments

Guerini

2022

Cells

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The cGAS STING pathway has received much attention in recent years, and it has been recognized as an important component of the innate immune response. Since the discovery of STING and that of cGAS, many observations based on preclinical models suggest that the faulty regulation of this pathway is involved in many type I IFN autoinflammatory disorders. Evidence has been accumulating that cGAS/STING might play an important role in pathologies beyond classical immune diseases, as in, for example, cardiac failure. Human genetic mutations that result in the activation of STING or that affect the activity of cGAS have been demonstrated as the drivers of rare interferonopathies affecting young children and young adults. Nevertheless, no data is available in the clinics demonstrating the therapeutic benefit in modulating the cGAS/STING pathway. This is due to the lack of STING/cGAS-specific low molecular weight modulators that would be qualified for clinical exploration. The early hopes to learn from STING agonists, which have reached the clinics in recent years for selected oncology indications, have not yet materialized since the initial trials are progressing very slowly. In addition, transforming STING agonists into potent selective antagonists has turned out to be more challenging than expected. Nevertheless, there has been progress in identifying novel low molecular weight compounds, in some cases with unexpected mode of action, that might soon move to clinical trials. This study gives an overview of some of the potential indications that might profit from modulation of the cGAS/STING pathway and a short overview of the efforts in identifying STING modulators (agonists and antagonists) suitable for clinical research and describing their potential as a “drug”.

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Juglanin alleviates bleomycin-induced lung injury by suppressing inflammation and fibrosis via targeting sting signaling

Cited by 33 publications

References 36 publications

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

STING Agonists/Antagonists: Their Potential as Therapeutics and Future Developments

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