The HMGB1-RAGE axis induces apoptosis in acute respiratory distress syndrome through PERK/eIF2α/ATF4-mediated endoplasmic reticulum stress

He, Fei; Gu, Lina; Cai, Nan; Ni, Jun; Liu, Yong; Zhang, Quan; Wu, Chao

doi:10.1007/s00011-022-01613-y

Cited by 5 publications

(4 citation statements)

References 39 publications

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“…and asthma, pulmonary fibrosis and other diseases. Studies have suggested that the association between acute lung injury, pulmonary edema, asthma and pulmonary cystic fibrosis may be related to the abnormal expression and function of HMGB1-RAGE ( 37 , 38 ). Currently, there are limited studies available on lung injury induced by altitude hypoxia through the HMGB1/RAGE pathway ( 5 , 39 ), and only a previous study demonstrated that the HMGB1/RAGE pathway may be involved in hypoxia-induced kidney injury ( 40 ).…”

Section: Introductionmentioning

confidence: 99%

Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia

Zhang¹,

Yan²,

Ge³

et al. 2023

Int J Mol Med

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High-altitude acute hypoxia is commonly associated with respiratory cardiovascular diseases. The inability to adapt to acute hypoxia may lead to cardiovascular dysfunction, lung injury and even death. Therefore, understanding the molecular basis of the adaptation to high-altitude acute hypoxia may reveal novel therapeutic approaches with which to counteract the detrimental consequences of hypoxia. In the present study, a high-altitude environment was simulated in a rat model in order to investigate the role of the high mobility group protein-1 (HMGB1)/receptor for advanced glycation end products (RAGE)/NF-κB and F2/Rho signaling pathways in lung injury induced by acute hypoxia. It was found that acute hypoxia caused inflammation through the HMGB1/RAGE/NF-κB pathway and coagulation dysfunction through the F2/Rho pathway, both of which may be key processes in acute hypoxia-induced lung injury. The present study provides new insight into the molecular basis of lung injury induced by acute hypoxia. The simultaneous activation of the HMGB1/RAGE/NF-κB and F2/Rho signaling pathways plays a critical role in hypoxia-induced inflammatory responses and coagulation abnormalities, and provides a theoretical basis for the development of potential therapeutic strategies.

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Section: Introductionmentioning

confidence: 99%

Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia

Zhang¹,

Yan²,

Ge³

et al. 2023

Int J Mol Med

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“…Accumulating evidence has reported that JNK is implicated in fibrosis by triggering several genes linked to inflammation and apoptosis 59 . Most importantly, some preceding studies have found that HMGB1 is the upstream regulator of ER stress; Huang et al 18 and He et al 19 demonstrated that HMGB1/RAGE interaction induced endothelial cell apoptosis and acute respiratory distress syndrome in patients and animals through activation of ER stress, respectively. In support of this observation, Lai et al 60 revealed that ER stress was attenuated by HMGB1 inhibition or neutralization in acute renal injury brought on by intestinal ischemia/reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…Emerging studies reported that ER stress is involved in diverse fibrotic disorders, such as lung fibrosis and chronic liver disease with fibrosis 16 , 17 . Prior studies have found that HMGB1 is the upstream regulator of ER stress 18 , 19 .…”

Section: Introductionmentioning

confidence: 99%

Diacerein ameliorates cholestasis-induced liver fibrosis in rat via modulating HMGB1/RAGE/NF-κB/JNK pathway and endoplasmic reticulum stress

Abdelfattah

Mahmoud

El-Wafaey

et al. 2023

Sci Rep

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Diacerein is an interleukin (IL)-1β inhibitor approved for osteoarthritis. This study aimed to investigate the potential anti-fibrotic effect of diacerein against bile duct ligation (BDL)-induced liver fibrosis. Forty male Wistar rats were divided into: sham-operated group, BDL group, and BDL groups treated with diacerein at 10, 30, and 50 mg/kg/day starting two days before surgery and continued for 4 weeks. Diacerein decreased the hepatic injury markers and alleviated oxidative stress triggered by BDL by reducing hepatic malondialdehyde (MDA) and increasing hepatic superoxide dismutase (SOD) levels. Diacerein mitigated BDL-induced inflammation via lowering hepatic levels and mRNA expression of high mobility group box 1 (HMGB1), nuclear factor-κB (NF-κB), and IL-1β. The hepatic gene expression of Advanced Glycation End products Receptor (RAGE) gene and immunohistochemical expression of some ER stress markers, e.g., glucose-regulated protein 78 (GRP78), inositol-requiring enzyme 1 (IRE1α), protein kinase RNA-like endoplasmic reticulum kinase (PERK), CCAAT/enhancer-binding protein homologous protein (CHOP), and phosphorylated c-Jun N-terminal kinase protein contents were lowered by diacerein. Furthermore, diacerein suppressed the hepatic levels of fibrogenic mediators, e.g., Transforming growth factor β1 (TGF˗β1), α- smooth muscle actin (α-SMA), collagen 1, and hydroxyproline, as well as the apoptotic caspase 3 and BAX immunostaining in BDL rats. The histopathological abnormalities induced by BDL significantly improved. Our study demonstrated that diacerein exhibited an antifibrotic effect by inhibiting HMGB1/RAGE/NF-κB/JNK pathway, and ER stress. Better protection was observed with increasing the dose.

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“…Specifically, HMGB1 can be secreted or released by stressed, dead, or dying cells ( Wang et al, 1999 ; Scaffidi et al, 2002 ; Zhu et al, 2021 ; Chen et al, 2022 ). Once released, HMGB1 acts as a damage-associated molecular pattern (DAMP) to trigger immune responses by binding multiple pattern recognition receptors, such as toll-like receptor 4 (TLR4) and advanced glycosylation end product-specific receptor (AGER, also known as RAGE) ( Tsung et al, 2007 ; Kang et al, 2014a ; Amornsupak et al, 2022 ; He et al, 2022 ; Lei et al, 2022 ). Targeting the release and activity of HMGB1 is an attractive strategy to limit excessive inflammation in diseases associated with microbial infection and tissue damage ( Andersson and Tracey, 2011 ; Kang et al, 2014b ; Andersson et al, 2021 ; Zhu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

HMGB1 is a mediator of cuproptosis-related sterile inflammation

Liu

Wang

et al. 2022

Front. Cell Dev. Biol.

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Cuproptosis is a recently recognized modality of cell death driven by intracellular copper-dependent mitochondrial stress. However, the mediators of the sterile inflammatory response to cuproptotic death are undetermined. Here, we report that high-mobility group box 1 (HMGB1), a damage-associated molecular pattern, is released by cuproptotic cells to initiate inflammation. Mechanically, copper accumulation-induced adenosine triphosphate (ATP) depletion activates AMP-activated protein kinase (AMPK) to promote HMGB1 phosphorylation, resulting in increased extracellular release. In contrast, genetic (using RNAi) or pharmacologic (using dorsomorphin) inhibition of AMPK activation limits cuproptosis and HMGB1 release. Functionally, the ability of HMGB1-deficient cuproptotic cells to promote advanced glycosylation end product-specific receptor (AGER, also known as RAGE)-dependent inflammatory cytokine production is greatly reduced. Thus, HMGB1 is a key immune mediator of cuproptosis-initiated sterile inflammation.

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The HMGB1-RAGE axis induces apoptosis in acute respiratory distress syndrome through PERK/eIF2α/ATF4-mediated endoplasmic reticulum stress

Cited by 5 publications

References 39 publications

Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia

Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia

Diacerein ameliorates cholestasis-induced liver fibrosis in rat via modulating HMGB1/RAGE/NF-κB/JNK pathway and endoplasmic reticulum stress

HMGB1 is a mediator of cuproptosis-related sterile inflammation

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