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HMGB1 induced endothelial permeability promotes myocardial fibrosis in diabetic cardiomyopathy
IJCA-21556; No of Pages 1 International Journal of Cardiology xxx (2015) xxx
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
HMGB1 induced endothelial permeability promotes myocardial fibrosis in diabetic cardiomyopathy Zhaowei Zhu 1, Xinqun Hu ⁎,1 Department of Cardiology, Second Xiangya Hospital of Central South University, Changsha, China
a r t i c l e
i n f o
Article history: Received 31 October 2015 Accepted 4 November 2015 Available online xxxx Keywords: HMGB1 Endothelial cell Myocardial fibrosis
HMGB1 levels have been found increased in T2DM patients than that in a control group [3]. At last, increased HMGB1 can induce intrinsic inflammation which will augment the cell stress, and we have found that HMGB1 can damage the endothelial cell permeability through TLR4/Caveolin-1 pathway [4], obviously, this damage will aggravate microvessel dysfunction, and enhanced ischemia can promote more myocardial fibrosis. Besides, although the authors have completed their work with lentivirus-mediated short-hairpin RNA in vivo, it will be better with conditional HMGB1 knockout animals. Conflict of interest
Dear Editor: We have recently read with great interest the report by Wen-ke Wang et al. [1] concerning “Inhibition of high-mobility group box 1 improves myocardial fibrosis and dysfunction in diabetic cardiomyopathy”. They indicate that HMGB1 inhibition could alleviate cardiac fibrosis and remodeling in diabetic cardiomyopathy. Inhibition of HMGB1 might have therapeutic potential in the treatment of the disease. In this paper, the authors have found that administration of rHMGB1 dose-dependently increased the expression of fibrosis markers: collagens I and III and TGF-β1 in cardiac fibroblasts which contribute most to this process. Based on our own work, we think it is possible that endothelial cell may also participate in HMGB1-mediated cardiac fibrosis. The reasons are as follows: First, macrovascular complications have been seen as a result of diabetes, and because endothelial cells are the major cell type in microvessel, this can be attributed a lot to endothelial cells [2]. Usually, such microvessel dysfunction can cause ischemia-induced cardiomyopathy where myocardial fibrosis happens. Secondly, in clinic, plasma
The authors report no relationships that could be construed as a conflict of interest. Sources of funding This work was supported in part by the National Natural Science Foundation of China (NSFC) projects 81470017 (to XQH). References [1] W.K. Wang, B. Wang, Q.H. Lu, Zhang, et al., Inhibition of high-mobility group box 1 improves myocardial fibrosis and dysfunction in diabetic cardiomyopathy, Int. J. Cardiol. 172 (2014) 202–212. [2] J.M. Forbes, M.E. Cooper, Mechanisms of diabetic complications, Physiol. Rev. 93 (2013) 137–188. [3] H. Wang, H. Qu, H. Deng, Plasma HMGB-1 levels in subjects with obesity and type 2 diabetes: a cross-sectional study in China, PLoS One 10 (2015), e0136564. [4] R. Jiang, J. Cai, Z. Zhu, et al., Hypoxic trophoblast HMGB1 induces endothelial cell hyperpermeability via the TRL-4/caveolin-1 pathway, J. Immunol. 193 (2014) 5000–5012.
⁎ Corresponding author at: Department of Cardiology, Second Xiangya Hospital of Central South University, middle Ren-Min road No.139, Changsha, Hunan 410011, China. E-mail address: [email protected] (X. Hu). 1 All of the authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
http://dx.doi.org/10.1016/j.ijcard.2015.11.024 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Z. Zhu, X. Hu, HMGB1 induced endothelial permeability promotes myocardial fibrosis in diabetic cardiomyopathy, Int J Cardiol (2015), http://dx.doi.org/10.1016/j.ijcard.2015.11.024
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
HMGB1 induced endothelial permeability promotes myocardial fibrosis in diabetic cardiomyopathy Zhaowei Zhu 1, Xinqun Hu ⁎,1 Department of Cardiology, Second Xiangya Hospital of Central South University, Changsha, China
a r t i c l e
i n f o
Article history: Received 31 October 2015 Accepted 4 November 2015 Available online xxxx Keywords: HMGB1 Endothelial cell Myocardial fibrosis
HMGB1 levels have been found increased in T2DM patients than that in a control group [3]. At last, increased HMGB1 can induce intrinsic inflammation which will augment the cell stress, and we have found that HMGB1 can damage the endothelial cell permeability through TLR4/Caveolin-1 pathway [4], obviously, this damage will aggravate microvessel dysfunction, and enhanced ischemia can promote more myocardial fibrosis. Besides, although the authors have completed their work with lentivirus-mediated short-hairpin RNA in vivo, it will be better with conditional HMGB1 knockout animals. Conflict of interest
Dear Editor: We have recently read with great interest the report by Wen-ke Wang et al. [1] concerning “Inhibition of high-mobility group box 1 improves myocardial fibrosis and dysfunction in diabetic cardiomyopathy”. They indicate that HMGB1 inhibition could alleviate cardiac fibrosis and remodeling in diabetic cardiomyopathy. Inhibition of HMGB1 might have therapeutic potential in the treatment of the disease. In this paper, the authors have found that administration of rHMGB1 dose-dependently increased the expression of fibrosis markers: collagens I and III and TGF-β1 in cardiac fibroblasts which contribute most to this process. Based on our own work, we think it is possible that endothelial cell may also participate in HMGB1-mediated cardiac fibrosis. The reasons are as follows: First, macrovascular complications have been seen as a result of diabetes, and because endothelial cells are the major cell type in microvessel, this can be attributed a lot to endothelial cells [2]. Usually, such microvessel dysfunction can cause ischemia-induced cardiomyopathy where myocardial fibrosis happens. Secondly, in clinic, plasma
The authors report no relationships that could be construed as a conflict of interest. Sources of funding This work was supported in part by the National Natural Science Foundation of China (NSFC) projects 81470017 (to XQH). References [1] W.K. Wang, B. Wang, Q.H. Lu, Zhang, et al., Inhibition of high-mobility group box 1 improves myocardial fibrosis and dysfunction in diabetic cardiomyopathy, Int. J. Cardiol. 172 (2014) 202–212. [2] J.M. Forbes, M.E. Cooper, Mechanisms of diabetic complications, Physiol. Rev. 93 (2013) 137–188. [3] H. Wang, H. Qu, H. Deng, Plasma HMGB-1 levels in subjects with obesity and type 2 diabetes: a cross-sectional study in China, PLoS One 10 (2015), e0136564. [4] R. Jiang, J. Cai, Z. Zhu, et al., Hypoxic trophoblast HMGB1 induces endothelial cell hyperpermeability via the TRL-4/caveolin-1 pathway, J. Immunol. 193 (2014) 5000–5012.
⁎ Corresponding author at: Department of Cardiology, Second Xiangya Hospital of Central South University, middle Ren-Min road No.139, Changsha, Hunan 410011, China. E-mail address: [email protected] (X. Hu). 1 All of the authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
http://dx.doi.org/10.1016/j.ijcard.2015.11.024 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Z. Zhu, X. Hu, HMGB1 induced endothelial permeability promotes myocardial fibrosis in diabetic cardiomyopathy, Int J Cardiol (2015), http://dx.doi.org/10.1016/j.ijcard.2015.11.024