High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives
Abstract
:1. Introduction
2. Diabetes Mellitus
3. HMGB1 and Diabetes
3.1. The Role of RAGE
3.2. The Role of TLRs
4. Diabetic Macroangiopathy
5. HMGB1 and Diabetic Coronary Artery Disease
6. HMGB1, Diabetes Mellitus and Peripheral Arterial Disease
7. HMGB1 and Diabetic Cerebrovascular Disease
8. Diabetic Microangiopathy
9. HMGB1 and Diabetic Nephropathy
10. HMGB1 and Diabetic Neuropathy
11. HMGB1 and Diabetic Retinopathy
12. HMGB1 and Diabetic Cardiomyopathy
13. Conclusions
Author Contributions
Funding
Conflicts of Interest
References
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Ref. | Year | Aim | HMGB1 |
---|---|---|---|
Yan et al. | 2009 | Role of HMGB1 in T2DM patients with CAD e in non-T2DM patients with CAD. | Increased serum levels of HMGB1 and hsCRP in non-T2DM patients with CAD and in T2DM patients with CAD. HMGB1 levels correlate with hsCRP, TNF-α, IL-6 levels. |
Yamashita et al. | 2012 | Presence of CD34-positive cells and HMGB1 in acute coronary thrombi in T2DM patients vs non-T2DM patients. | Extracellular HMGB1 area in the thrombi larger in T2DM patients. HMGB1 facilitates thrombus formation. |
Yin et al. | 2015 | Relationship between blood glucose levels and HMGB1 levels T2DM patients with CAD. | Increased serum levels of HMGB1 in T2DM patients with CAD. Levels of HMGB1 correlate with glucose levels and HbA1c levels. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
Biscetti et al. | 2010 | Role of HMGB1 in diabetic angiogenesis. | Lower HMGB1 protein expression in the ischemic tissue of STZ-induced mice. HMGB1 administration ameliorates the blood flow recovery and capillary density in the ischemic muscle of STZ-induced mice. Reduced HMGB1-induced angiogenesis by inhibiting VEGF activity. |
Tsao et al. | 2015 | Expression of HMGB1 in diabetic foot atherogenesis. | Increased HMGB1 expression in vessels of T2DM patients and T2DM patients with PAD compared to non-T2DM patients. |
Giovannini et al. | 2017 | Role of HMGB1, OPG, TNF-α, IL-6, CRP in diabetic patients with PAD. | Increased serum levels of HMGB1 in T2DM patients with PAD. Levels of HMGB1 positively correlates with severity of PAD in T2DM patients. HMGB1 independent risk factor for PAD in T2DM patients. |
Biscetti et al. | 2017 | Role of HMGB1 in cell therapy with HASCs in PAD. | Improved blood flow recovery in mice co-treated with HASCs and HMGB1 protein, compared to HASCs-treated mice. Reduced post-ischemic angiogenesis with HMGB1 inhibition in mice co-treated with HASCs and HMGB1. |
Hafez et al. | 2018 | Role of Sirtuin-1 and HMGB1 in DFU. | Increased serum levels HMGB1 and AGEs in T2DM patients compared to non-T2DM patients with the highest levels in T2DM patients with DFU. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
Ye et al. | 2011 | Role of HMGB1 and RAGE in stroke in T1DM rats and role of niaspan on pro-inflammatory proteins expression. | Increased HMGB1 expression after stroke in brains of STZ-induced MCAo rats. Niaspan treatment in STZ-induced MCAo rats decreased HMGB1 expression. |
Hu et al. | 2016 | Role of HMGB1 in stroke in T2DM rats and role of BMSCs in HMGB1 inflammation. | MCAo STZ/N-induced rats: increased HMGB1 and RAGE expression, increased BBB leakage, decreased functional outcome after stroke. Injection of BMSCs in STZ/N-induced rats: decreased HMGB1 and RAGE expression, attenuated BBB leakage and improved functional outcome after stroke, decreased inflammation after stroke. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
Kim et al. | 2011 | Role of HMGB1, RAGE and NF-kB in DN. | Increased HMGB1 levels in cytoplasmic and nuclear patterns of glomerular cells of STZ-induced rats vs non STZ-induced rats (nuclear HMGB1 only). |
Lin et al. | 2012 | Role of TLR-4 in DN. | Increased HMGB1 expression in renal biopsies of T2DM patients with DN. |
Mudaliar et al. | 2013 | Role of TLR-2 and -4 in DN. | Upregulation of HMGB1 and TLR-2 levels in tubules cells of STZ-induced mice compared to non STZ induced mice. Increased HMGB1 secretion and NF-kB activation in response to high level of glucose. Reduced HMGB1 secretion and NF-kB activation with TLR-2 siRNA and TLR-4 siRNA. |
Ma et al. | 2014 | Role of TLR-4 in DN. | Upregulation of HMGB1 in STZ-induced WT mice and STZ-induced TLR-4 deficient mice compared to non STZ-induced mice. |
Ma et al. | 2014 | Role of TLR-2 in DN. | Upregulation of HMGB1 in STZ-induced WT mice compared to non STZ-induced WT mice. |
Chen et al. | 2015 | Role of high glucose on HMGB1 expression in T2DM patients and in mesangial cells. | Increased serum HMGB1 levels in T2DM patients and in mesangial cells stimulated with high glucose. Knockdown of HMGB1 in mesangial cells reduces HMGB1 mRNA levels. |
Zhang et al. | 2017 | Role of HMGB1 inhibitor GA in DN. | Increased HMGB1 expression in kidney tissue of STZ-induced rats and lower HMGB1 expression in kidney tissue of STZ-induced rats treated with GA. |
Jigheh et al. | 2018 | Empaglifozin role in reduction of HMGB1 and TLR-4 levels in DN. | Empaglifozin reduces renal levels of HMGB1 in STZ-induced rats. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
El Asrar et al. | 2014 | Role of HMGB1 in retinal neuropathy. | Increased HMGB1 retinal levels in STZ-induced rats. Vitreal injection of HMGB1in non STZ-induced rats increased HMGB1 mRNA levels. GA intake in STZ-induced rats decreased HMGB1 mRNA levels. |
Meng et al. | 2015 | GWAS to clarify the role of sex specific involvement of Chr1p35.1 (ZSCAN-TLR12P) and Chr8p23.1 (HMGB1P46) in diabetic NP. | Involvement of Chr8p23.1 (HMGB1P46) in NP, with high heritability of Chr8p23.1 (HMGB1P46) in males. |
Zhao et al. | 2015 | Role of HMGB1 in RGC in high glucose environment. | Increased levels of HMGB1 mRNA and protein in RGC and decreased cells survival in high glucose environment. Decreased levels of HMGB1 mRNA and protein in RGC and increased cells survival after siRNA HMGB1 injection. |
Zhao et al. | 2016 | Role of CaMKIV in diabetic NP and its relationship with HMGB1 expression in DRG. | Increased pCAMKIV and HMGB1 levels in DRG of STZ-induced rats. Inhibition of CAMKIV reduced CAMKIV and HMGB1 expression in DRG of STZ-induced rats. |
Wang et al. | 2018 | Role of sigma 1 receptor and its relationship with HMGB1 expression in DRG in NP. | In STZ-induced rats TA and TH correlate with increased HMGB1 expression in DRG. Stimulation of Sigma-1R induces TA and TH and increases HMGB1 levels. Blockade of Sigma-1R and HMGB1 reduce TA and TH. STZ-induced Sigma-1R knockdown rats have modest NP and no variation in HMGB1 levels. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
El-Asrar et al. | 2011 | Levels of HMGB1, RAGE in patients with PDR and correlation with MCP-1, sICAM-1, IL-1 beta, GM-CSF. | Increased HGMB1 levels in vitreous samples of patients with PDR. Increased HMGB1 levels in patients with PDR and hemorrhages. |
El-Asrar et al. | 2012 | Levels of HMGB1 in patients with PDR and correlation with VEGF, G-CSF, sVE-cadherin, sEng. | Increased HMGB1 levels in vitreous samples of patients with PDR. |
Mohammad et al. | 2012 | Role of HMGB1 in DR. | Increased HMGB1 levels in retinas of STZ-induced rats. Intravitreal administration of HMGB1 in non STZ-induced rats increases levels of ICAM-1, sICAM-1, HMGB1, RAGE, ERK1/2, NFkB and retinal permeability. Administration of GA reduced upregulation of HMGB1 in STZ-induced rats. |
Gong et al. | 2014 | Role of HMGB1 and PLA2 in DR. | Increased HMGB1 levels in retinal tissue of STZ-induced rats; HMGB1 induces endothelial cells death directly and pericytes death through cytotoxic activity of glial cells. |
Santos et al. | 2014 | Role of HMGB1 in vulnerability of endothelial cells and pericytes. | HMGB1 induces endothelial cells death directly and pericytes death through glial cells. No differences between neovascularization and levels of VEGF after HMGB1 subretinal administration. No involvement of HMGB1 in rats with oxygen induced retinopathy. |
Fu et al. | 2015 | Serum HMGB1 and VEGF levels in DR patients. | Increased serum HMGB1 levels in DR patients. In vitro HMGB1 inhibits human retina pigment epithelium cells growth and it induces apoptosis. |
Mohammad et al. | 2015 | Relationship between HMGB1 and NADPH oxidase-derived ROS in DR. | Increased HMGB1 levels and oxidative stress in vitreous fluid of PDR patients. HMGB1 enhances IL-1β, ROS, Nox2, PARP-1, and cleaved caspase-3 production by HRMEC. Diabetes and intra-vitreal injection of HMGB1 in normal rats induce significant upregulation of ROS, Nox2, PARP-1, and cleaved caspase-3 in the retina. |
Yu et al. | 2015 | Role of HMGB1 in DR inflammation and cellular apoptosis. | Increased HMGB1 expression in retinas of STZ-induced rats. HMGB1 accelerates apoptosis of diabetic retinal cells. |
Kim et al. | 2016 | Role of HMGB1, RAGE, NFkB in DR. | Increased HMGB1 cytoplasmic translocation in high glucose environment. |
Jiang et al. | 2016 | Role of HMGB1 and TLR-9 in DR. | Increased HMGB1 and TLR-9 expression in retinas tissues and in RGC of STZ-induced rats. |
Sohn et al. | 2016 | Protective effect of PCE in DR by inhibition of HMGB1 pathway. | Increased levels of HMGB1 in retinas of STZ-induced rats. Treatment with PCE reduces HMGB1 and RAGE expression in retinas of STZ-rats. |
Chang et al. | 2017 | Role of hypoxia in HMGB1 release in DR. | Hypoxia induces HMGB1 cytoplasmic release. HMGB1 upregulates expression of VEGF, bFGF, TGF-β2, CTCF and phosphorylation of Akt, p38MAPK and NFkB but not ERK, JNK, Smad2. HMGB1 causes growth suppression and G1 cell cycle arrest in ARPE-19 cells. Neutralization of TLR4 and RAGE reduces HMGB1-driven cytokines production. |
Jiang et al. | 2017 | Role of HMGB1siRNA in DR. | HMGB1siRNA reduces apoptosis and oxidative damage of retinal cells in STZ-induced rats (intravitreal injection) and in HRECs (HMGBsiRNA pre-treatment) of treated with high. Decreased IKKβ and NFκB protein expression after HMGB1 silencing. |
Jiang et al. | 2018 | Role of HMGB1on the proteins involved in insulin signaling. | Recombinant HMGB1 blocks insulin receptor and Akt phosphorylation through RAGE and TLR-4. |
Liu et al. | 2018 | Role of PKA in HMGB1 inhibition. | PKA inhibits cytoplasmic HMGB1, activating IGFBP-3 and SIRT1. |
Zhang et al. | 2018 | Role of exosome derived from mesenchymal stem cells in retinal inflammation reduction. | MSC-exos overexpressing miR-126 suppresses HMGB1 expression and NLRP3 inflammasome activity in human retinal endothelial cells. |
Ref. | Year | Aim | HMGB1 |
---|---|---|---|
Volz et al. | 2010 | Role of HMGB1 in diabetic heart disease. | High glucose treatment of cardiac fibroblasts, macrophages and cardiomyocytes increased HMGB1 mRNA expression and protein levels. Increased cardiac HMGB1 mRNA expression and protein levels in STZ-induced mice with post-myocardial infarction remodeling and HMGB1 blockage reduces post-myocardial infarction remodeling and markers of tissue damage. |
Wang et al. | 2014 | Role of HMGB1 in high glucose-induced apoptosis of cardiomyocytes. | HMGB1siRNA reduces cell apoptosis in high glucose milieu through Ets-1/ERK1/2 signaling. |
Wang et al. | 2014 | Role of HMGB1 in fibrosis and myocardial dysfunction. | HMGB1 silencing ameliorated LV dysfunction and remodeling in STZ-induced mice. High glucose milieu induced HMGB1 translocation and secretion in isolated cardiac fibroblasts. Administration of HMGB1 increased expression of collagens I and III and TGF-β1 in cardiac fibroblasts. HMGB1 inhibition reduced high glucose-induced collagen production, MMP activity, proliferation, MAPK signaling. |
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Biscetti, F.; Rando, M.M.; Nardella, E.; Cecchini, A.L.; Pecorini, G.; Landolfi, R.; Flex, A. High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives. Int. J. Mol. Sci. 2019, 20, 6258. https://doi.org/10.3390/ijms20246258
Biscetti F, Rando MM, Nardella E, Cecchini AL, Pecorini G, Landolfi R, Flex A. High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives. International Journal of Molecular Sciences. 2019; 20(24):6258. https://doi.org/10.3390/ijms20246258
Chicago/Turabian StyleBiscetti, Federico, Maria Margherita Rando, Elisabetta Nardella, Andrea Leonardo Cecchini, Giovanni Pecorini, Raffaele Landolfi, and Andrea Flex. 2019. "High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives" International Journal of Molecular Sciences 20, no. 24: 6258. https://doi.org/10.3390/ijms20246258