The role of high mobility group box 1 protein in acute cerebrovascular diseases (Review)

Mu, Shuwen; Dang, Yuan; Wang, Shousen; Gu, Jianjun

doi:10.3892/br.2018.1127

Cited by 14 publications

(14 citation statements)

References 63 publications

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“…In the initial stage of cerebrovascular and cardiovascular diseases, HMGB1 is released from the cell to participate in the cascade amplification reaction of inflammation, causing vasospasm and apoptosis [ 20 , 41 , 42 ]. In the recovery stage of disease, HMGB1 can promote tissue repair, regeneration, and remodelling [ 20 , 41 , 42 ]. It is necessary to investigate whether the newly generated HMGB1 plays a role in propagating inflammatory detriment or repairing damages over time after injury.…”

Section: Discussionmentioning

confidence: 99%

Targeted temperature management at 33°C or 36℃ induces equivalent myocardial protection by inhibiting HMGB1 release in myocardial ischemia/reperfusion injury

et al. 2021

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Acute myocardial infarction (AMI) is lethal and causes myocardial necrosis via time-dependent ischemia due to prolonged occlusion of the infarct-related artery. No effective therapy or potential therapeutic targets can prevent myocardial ischemia/reperfusion (I/R) injury. Targeted temperature management (TTM) may reduce peri-infarct regions by inhibiting the extracellular release of high mobility group box-1 (HMGB1) as a primary mediator of the innate immune response. We used a rat left anterior descending (LAD) coronary artery ligation model to determine if TTM at 33°C and 36°C had similar myocardial protective effects. Rats were divided into sham, LAD I/R+37°C normothermia, LAD I/R+33°C TTM, and LAD I/R+36°C TTM groups (n = 5 per group). To verify the cardioprotective effect of TTM by specifically inhibiting HMGB1, rats were assigned to sham, LAD I/R, and LAD I/R after pre-treatment with glycyrrhizin (known as a pharmacological inhibitor of HMGB1) groups (n = 5 per group). Different target temperatures of 33°C and 36°C caused equivalent reductions in infarct volume after myocardial I/R, inhibited the extracellular release of HMGB1 from infarct tissue, and suppressed the expression of inflammatory cytokines from peri-infarct regions. TTM at 33°C and 36°C significantly attenuated the elevation of cardiac troponin, a sensitive and specific marker of heart muscle damage, after injury. Similarly, glycyrrhizin alleviated myocardial damage by suppressing the extracellular release of HMGB1. TTM at 33°C and 36°C had equivalent myocardial protective effects by similar inhibiting HMGB1 release against myocardial I/R injury. This is the first study to suggest that a target core temperature of 36°C is applicable for cardioprotection.

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Section: Discussionmentioning

confidence: 99%

Targeted temperature management at 33°C or 36℃ induces equivalent myocardial protection by inhibiting HMGB1 release in myocardial ischemia/reperfusion injury

et al. 2021

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“…HMGB1 can trigger downstream inflammatory responses in CI/RI model. In the process, HMGB1 triggers three specific downstream receptors, RAGE, TLR-2 and TLR-4 ( 106 ), which further induce the expression of NF-κB, MMP, and MAPK ( 107 , 108 ). The inflammatory cascade is involved in BBB disruption, apoptosis and nerve damage, and further aggravating brain damage.…”

Section: The Role Of Pparγ In Maintaining the Bbb During Ci/rimentioning

confidence: 99%

“…The inflammatory cascade is involved in BBB disruption, apoptosis and nerve damage, and further aggravating brain damage. Anti-HMGB1 antibody can inhibit the morphological and functional changes in the BBB induced by HMGB1 ( 106 ). Telmisartan significantly decreased the number of Iba1-positive cells expressing HMGB1 and decreased plasma HMGB1 levels in PPARγ-dependent manner, thus improving BBB damage ( 109 ).…”

Section: The Role Of Pparγ In Maintaining the Bbb During Ci/rimentioning

confidence: 99%

The Protective Effects of Peroxisome Proliferator-Activated Receptor Gamma in Cerebral Ischemia-Reperfusion Injury

et al. 2020

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Cerebral ischemia-reperfusion injury (CI/RI) is a complex pathological process that often occurs secondary to trauma, surgery, and shock. Peroxisome proliferator activated receptor gamma (PPARγ) is a subunit of the PPAR and is a ligand-activated nuclear transcription factor. After being activated by its ligand, PPARγ can combine with specific DNA response elements to regulate the transcription and expression of genes. It has a wide range of biological functions, such as regulating lipid metabolism, improving insulin sensitivity, modulating anti-tumor mechanisms, and inhibiting inflammation. In recent years, some studies have shown that PPARγ exerts a protective effect during CI/RI. This article aims to summarize the research progress of studies that have investigated the protective effects of PPARγ in CI/RI and the cellular and molecular mechanisms through which these effects are modulated, including inhibition of excitatory amino acid toxicity, reduced Ca 2+ overload, anti-oxidative stress, anti-inflammation, inhibition of microglial activation, maintain the BBB, promotion of angiogenesis, and neurogenesis and anti-apoptotic processes.

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“…Necrotic or apoptotic cells release DAMPs after stroke, which consist of a various substances, such as purines (ATP and UTP), high mobility group binding protein 1 (HMGB1), heat shock proteins (HSPs), peroxiredoxins and mitochondrial-derived N-formyl peptides [6,13]. DAMPs activate microglia and peripheral innate immune cells by binding to specific PRRs on the cell surface [14].…”

Section: The Immune Response In the Natural History Of Ichmentioning

confidence: 99%

Emerging therapeutic targets associated with the immune system in patients with intracerebral haemorrhage (ICH): From mechanisms to translation

Shao

Zhu

et al. 2019

EBioMedicine

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Intracranial haemorrhage (ICH) is a life-threatening type of stroke with high mortality, morbidity, and recurrence rates. However, no effective treatment has been established to improve functional outcomes in patients with ICH to date. Strategies targeting secondary brain injury are of great interest in both experimental and translational studies. The immune system is increasingly considered to be a crucial contributor to ICH-induced brain injury because it participates in multiple phases of ICH, from the early vascular rupture events to brain recovery. Various pathobiological processes that contribute to secondary brain injury closely interact with the immune system, such as brain oedema, neuroinflammation, and neuronal damage. Hence, we summarize the immune response to ICH and recent progress in treatments targeting the immune system in this review. The emerging therapeutic strategies that target the immune system after ICH are a particular focus and have been summarized.

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The role of high mobility group box 1 protein in acute cerebrovascular diseases (Review)

Cited by 14 publications

References 63 publications

Targeted temperature management at 33°C or 36℃ induces equivalent myocardial protection by inhibiting HMGB1 release in myocardial ischemia/reperfusion injury

Targeted temperature management at 33°C or 36℃ induces equivalent myocardial protection by inhibiting HMGB1 release in myocardial ischemia/reperfusion injury

The Protective Effects of Peroxisome Proliferator-Activated Receptor Gamma in Cerebral Ischemia-Reperfusion Injury

Emerging therapeutic targets associated with the immune system in patients with intracerebral haemorrhage (ICH): From mechanisms to translation

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