Targeting circulating high mobility group box-1 and histones by extracorporeal blood purification as an immunomodulation strategy against critical illnesses

Li, Yupei; Chen, Yu; Yang, Tinghang; Chang, Kaixi; Deng, Ningyue; Zhao, Weifeng; Su, Baihai

doi:10.1186/s13054-023-04382-0

Cited by 14 publications

(15 citation statements)

References 115 publications

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“…Based on previous reports, endogenous HMGB1 mediates ferroptosis and autophagy ( 21 ). HMGB1 was found to be knocked down in hypoxic macrophages ( Supplementary Figure 6A ).…”

Section: Resultsmentioning

confidence: 92%

IL6/adiponectin/HMGB1 feedback loop mediates adipocyte and macrophage crosstalk and M2 polarization after myocardial infarction

Zheng,

Wang,

et al. 2024

Front. Immunol.

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BackgroundDifferences in border zone contribute to different outcomes post-infarction, such as left ventricular aneurysm (LVA) and myocardial infarction (MI). LVA usually forms within 24 h of the onset of MI and may cause heart rupture; however, LVA surgery is best performed 3 months after MI. Few studies have investigated the LVA model, the differences in border zones between LVA and MI, and the mechanism in the border zone.MethodsThe LVA, MI, and SHAM mouse models were used. Echocardiography, Masson’s trichrome staining, and immunofluorescence staining were performed, and RNA sequencing of the border zone was conducted. The adipocyte-conditioned medium-treated hypoxic macrophage cell line and LVA and MI mouse models were employed to determine the effects of the hub gene, adiponectin (ADPN), on macrophages. Quantitative polymerase chain reaction (qPCR), Western blot analysis, transmission electron microscopy, and chromatin immunoprecipitation (ChIP) assays were conducted to elucidate the mechanism in the border zone. Human subepicardial adipose tissue and blood samples were collected to validate the effects of ADPN.ResultsA novel, simple, consistent, and low-cost LVA mouse model was constructed. LVA caused a greater reduction in contractile functions than MI owing to reduced wall thickness and edema in the border zone. ADPN impeded cardiac edema and promoted lymphangiogenesis by increasing macrophage infiltration post-infarction. Adipocyte-derived ADPN promoted M2 polarization and sustained mitochondrial quality via the ADPN/AdipoR2/HMGB1 axis. Mechanistically, ADPN impeded macrophage HMGB1 inflammation and decreased interleukin-6 (IL6) and HMGB1 secretion. The secretion of IL6 and HMGB1 increased ADPN expression via STAT3 and the co-transcription factor, YAP, in adipocytes. Based on ChIP and Dual-Glo luciferase experiments, STAT3 promoted ADPN transcription by binding to its promoter in adipocytes. In vivo, ADPN promoted lymphangiogenesis and decreased myocardial injury after MI. These phenotypes were rescued by macrophage depletion or HMGB1 knockdown in macrophages. Supplying adipocytes overexpressing STAT3 decreased collagen disposition, increased lymphangiogenesis, and impaired myocardial injury. However, these effects were rescued after HMGB1 knockdown in macrophages. Overall, the IL6/ADPN/HMGB1 axis was validated using human subepicardial tissue and blood samples. This axis could serve as an independent factor in overweight MI patients who need coronary artery bypass grafting (CABG) treatment.ConclusionThe IL6/ADPN/HMGB1 loop between adipocytes and macrophages in the border zone contributes to different clinical outcomes post-infarction. Thus, targeting the IL6/ADPN/HMGB1 loop may be a novel therapeutic approach for cardiac lymphatic regulation and reduction of cell senescence post-infarction.

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“…Based on previous reports, endogenous HMGB1 mediates ferroptosis and autophagy ( 21 ). HMGB1 was found to be knocked down in hypoxic macrophages ( Supplementary Figure 6A ).…”

Section: Resultsmentioning

confidence: 92%

IL6/adiponectin/HMGB1 feedback loop mediates adipocyte and macrophage crosstalk and M2 polarization after myocardial infarction

Zheng,

Wang,

et al. 2024

Front. Immunol.

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“…Li et al . [ 68 ] used hydrogel microspheres made of polyethersulfone designed to bind intrinsic coagulation factors, calcium ions, and inflammatory histones to modulate dysregulated inflammation and thrombosis. They are investigating the use of anticoagulant hydrogel microspheres to reduce histones and inflammation in large animal models of sepsis.…”

Section: Discussionmentioning

confidence: 99%

AKI in adults with COVID-19 infection: Mechanisms of development and role of blood filtration devices in treatment

Bansal,

Hu,

Raina

et al. 2023

Indian J Nephrol

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During the coronavirus disease 2019 (COVID-19) pandemic, acute kidney injury (AKI) was a common sequela of COVID-19 infection and predicted disease severity and mortality. Extracorporeal blood purification techniques involving blood filtration devices are an emerging treatment for AKI in the setting of severe COVID-19 infections. In this review, we discuss potential mechanisms for the development of AKI in COVID-19 patients as well as the various available blood filtration devices and the role they may play in managing the AKI in COVID-19 patients. A total of seven blood filters currently available were compared based on their potential in treating AKI in COVID-19 patients. Blood filtration devices show potential as an emerging treatment modality for COVID-19–induced AKI, but further clinical trials are necessary before their widespread adoption and usage.

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“…HMGB1 can be cleared by hemofiltration and hemodialysis using super-high-flux or high-cutoff membranes 139 . Therefore, the targeted clearance of HMGB1 by in vitro blood purification might effectively improve the clinical outcomes of critically ill patients, including ESRD 140 .…”

Section: Pathogenic Roles Of Hmgb1 In Ckdmentioning

confidence: 99%

Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease

Liu,

Li,

Jin

et al. 2023

Int. J. Biol. Sci.

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High-mobility group protein box 1 (HMGB1) is a member of a highly conserved high-mobility group protein present in all cell types. HMGB1 plays multiple roles both inside and outside the cell, depending on its subcellular localization, context, and post-translational modifications. HMGB1 is also associated with the progression of various diseases. Particularly, HMGB1 plays a critical role in CKD progression and prognosis. HMGB1 participates in multiple key events in CKD progression by activating downstream signals, including renal inflammation, the onset of persistent fibrosis, renal aging, AKI-to-CKD transition, and important cardiovascular complications. More importantly, HMGB1 plays a distinct role in the chronic pathophysiology of kidney disease, which differs from that in acute lesions. This review describes the regulatory role of HMGB1 in renal homeostasis and summarizes how HMGB1 affects CKD progression and prognosis. Finally, some promising therapeutic strategies for the targeted inhibition of HMGB1 in improving CKD are summarized. Although the application of HMGB1 as a therapeutic target in CKD faces some challenges, a more in-depth understanding of the intracellular and extracellular regulatory mechanisms of HMGB1 that underly the occurrence and progression of CKD might render HMGB1 an attractive therapeutic target for CKD.

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Targeting circulating high mobility group box-1 and histones by extracorporeal blood purification as an immunomodulation strategy against critical illnesses

Cited by 14 publications

References 115 publications

IL6/adiponectin/HMGB1 feedback loop mediates adipocyte and macrophage crosstalk and M2 polarization after myocardial infarction

IL6/adiponectin/HMGB1 feedback loop mediates adipocyte and macrophage crosstalk and M2 polarization after myocardial infarction

AKI in adults with COVID-19 infection: Mechanisms of development and role of blood filtration devices in treatment

Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease

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