- Email: [email protected]
Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure”
International Journal of Cardiology 187 (2015) 434–435
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure” Rui-Jie Gao a, Yan-Hong Zhou b, Tao Liu b, Qian-Feng Han b, Heng-Chen Yao b,⁎ a b
Department of Cardiology, Second People's Hospital of Weifang and Clinical School of Weifang Medical University, Weifang 261041, PR China Department of Cardiology, Liaocheng People's Hospital, and Clinical School of Taishan Medical University, Liaocheng 252000, PR China
a r t i c l e
i n f o
Article history: Received 24 March 2015 Accepted 25 March 2015 Available online 4 April 2015 Keywords: High mobility group box 1 Ischemic heart disease Endothelial cells
We thank Dr Zhu et al. for their interest in our study on the predictive value of increased high mobility group box 1 (HMGB1) levels in patients with chronic heart failure (HF) [1]. We have carefully read with great appreciation Dr Zhu and colleagues' article entitled endothelial cell is critical in HMGB1 mediated cardiac impairment in ischemic heart disease that was recently published in Int J Cardiol [2]. Yes, indeed, our article is just a clinical report without discussing related mechanisms by which increased HMGB1 may predict the fatal outcomes in patients with chronic HF. Because our purpose was only to emphasize the predictive value of HMGB1 in patients with chronic HF other than the underlying mechanisms. However, in frank, our study has one limitation that the study samples we recruited were a little small. Thus, further studies with large sample scales are needed to clarify the accurate predictive value in patients with chronic HF and also its mechanisms by which HMGB1 can take important roles in cardiovascular diseases, especially in chronic HF and in ischemic heart disease. Dr Zhu's group has proposed that endothelial cells may mediate the effect of HMGB1 in ischemic heart disease and has also given the associated reasons. We agree that endothelial cells may, at least in part, take important roles in mediating the myocardial impairment of HMGB1 in ischemic heart disease. However, as to the effects of HMGB1 in ischemic heart disease, lots of studies have been done in recent decades. Recently, we have found that serum levels of HMGB1 were significantly increased in patients with coronary artery disease and correlate with the severity of this disease [3]. Furthermore, we have also found that the myocardial expression of HMGB1 protein was elevated significantly in an acute ⁎ Corresponding author. E-mail address: [email protected] (H.-C. Yao).
http://dx.doi.org/10.1016/j.ijcard.2015.03.380 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
myocardial infarction rat model than in the sham group [4]. These clinical and basic research results suggest that increased HMGB1 was involved in the development and progress of ischemic heart disease. These are in accordance with some recent reported studies [5–7]. Recently, some studies have reported that exogenous HMGB1 protect heart against myocardial infarction [8] or myocardial ischemia reperfusion injury [9]. Thus HMGB1 may be a potential therapeutic target [10] both for basic myocardial ischemia and reperfusion injury research and clinical study in patients with ischemic heart disease. As to the underlying mechanisms that mediating HMGB1 in the impairment or protection in ischemic heart disease is multifactorial. The major mechanisms may involved with endothelial cells [2], PI3K/Akt signal pathway [11], hypoxia inducible factor-1α [12], heat shock protein β1 [13], angiogenesis [14], autophagy [15], nuclear factor kappa B [16] and so on. Although multiple mechanisms are likely involved in HMGB1 mediated pathophysiologic process in ischemic heart disease, further studies should be carried out to better understand the real meaning of HMGB1 in the future. Source of funding This work was supported by the Natural Science Foundation of Shandong Province (ZR2013HL017), the Natural Science Foundation of Liaocheng City (2012NS13), and the Scientific and Technologic Developing Project of Liaocheng City (2014GJH26). Conflict of interest None declared. References [1] T. Liu, Y. Zhang, Y.H. Zhou, Q.F. Han, L.H. Wang, L. Wu, H.C. Yao, Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure, Int. J. Cardiol. 184C (2015) 318–320. [2] Z. Zhu, X. Hu, Z. Fang, S. Zhou, Endothelial cell is critical in HMGB1 mediated cardiac impairment in ischemic heart disease, Int. J. Cardiol. 187 (2015) 39–40. [3] H.C. Yao, A.P. Zhao, Q.F. Han, L. Wu, D.K. Yao, L.X. Wang, Correlation between serum high-mobility group box-1 levels and high-sensitivity C-reactive protein and troponin I in patients with coronary artery disease, Exp. Ther. Med. 6 (2013) 121–124. [4] H.C. Yao, L.J. Yang, Q.F. Han, L.H. Wang, L. Wu, C.Y. Zhang, K.L. Tian, M. Zhang, Postconditioning with simvastatin decreases myocardial injury in rats following acute myocardial ischemia, Exp. Ther. Med. 9 (2015) 1166–1170. [5] X. Hu, X. Zhou, B. He, C. Xu, L. Wu, B. Cui, H. Wen, Z. Lu, H. Jiang, Minocycline protects against myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats, Eur. J. Pharmacol. 638 (2010) 84–89.
R.-J. Gao et al. / International Journal of Cardiology 187 (2015) 434–435 [6] X. Hu, H. Jiang, Q. Bai, X. Zhou, C. Xu, Z. Lu, B. Cui, H. Wen, Increased serum HMGB1 is related to the severity of coronary artery stenosis, Clin. Chim. Acta 406 (2009) 139–142. [7] Y. Lin, L. Chen, W. Li, J. Fang, Role of high-mobility group box-1 in myocardial ischemia/reperfusion injury and the effect of ethyl pyruvate, Exp. Ther. Med. 9 (2015) 1537–1541. [8] X. Zhou, X. Hu, J. Xie, C. Xu, W. Xu, H. Jiang, Exogenous high-mobility group box 1 protein injection improves cardiac function after myocardial infarction: involvement of Wnt signaling activation, J. Biomed. Biotechnol. 2012 (2012) 743879. [9] Y. Zhang, A.X. Zhang, Y.H. Zhou, L.H. Wang, H.C. Yao, Protection of intravenous HMGB1 on myocardial ischemia reperfusion injury, Int. J. Cardiol. 184C (2015) 280–282. [10] X. Hu, W. Fu, H. Jiang, HMGB1: a potential therapeutic target for myocardial ischemia and reperfusion injury, Int. J. Cardiol. 155 (2012) 489. [11] X. Hu, C. Xu, X. Zhou, B. Cui, Z. Lu, H. Jiang, PI3K/Akt signaling pathway involved in cardioprotection of preconditioning with high mobility group box 1 protein during myocardial ischemia and reperfusion, Int. J. Cardiol. 150 (2011) 222–223. [12] H.C. Yao, M. Zhou, Y.H. Zhou, L.H. Wang, D.Y. Zhang, Q.F. Han, T. Liu, L. Wu, K.L. Tian, M. Zhang, Intravenous high mobility group box 1 upregulates HIF-1α expression in
[13]
[14]
[15] [16]
435
ischemic reperfusion myocardium via a protein kinase B-dependent pathway in rats following acute myocardial ischemia, Mol. Med. Rep. (2015) (Accepted, in press). T. Narumi, T. Shishido, Y. Otaki, S. Kadowaki, Y. Honda, A. Funayama, S. Honda, H. Hasegawa, D. Kinoshita, M. Yokoyama, S. Nishiyama, H. Takahashi, T. Arimoto, T. Miyamoto, T. Watanabe, A. Tanaka, C.H. Woo, J.I. Abe, Y. Takeishi, I. Kubota, Highmobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis, J. Mol. Cell. Cardiol. 82 (2015) 11–12. Y. Nakamura, S. Suzuki, T. Shimizu, M. Miyata, T. Shishido, K. Ikeda, S.I. Saitoh, I. Kubota, Y. Takeishi, High mobility group box 1 promotes angiogenesis from bone marrow-derived endothelial progenitor cells after myocardial infarction, J. Atheroscler. Thromb. (Jan 22 2015) (Epub ahead of print). X. Sun, D. Tang, HMGB1-dependent and -independent autophagy, Autophagy 10 (2014) 1873–1876. H. Diao, Z. Kang, F. Han, W. Jiang, Astilbin protects diabetic rat heart against ischemia–reperfusion injury via blockade of HMGB1-dependent NF-κB signaling pathway, Food Chem. Toxicol. 63 (2014) 104–110.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure” Rui-Jie Gao a, Yan-Hong Zhou b, Tao Liu b, Qian-Feng Han b, Heng-Chen Yao b,⁎ a b
Department of Cardiology, Second People's Hospital of Weifang and Clinical School of Weifang Medical University, Weifang 261041, PR China Department of Cardiology, Liaocheng People's Hospital, and Clinical School of Taishan Medical University, Liaocheng 252000, PR China
a r t i c l e
i n f o
Article history: Received 24 March 2015 Accepted 25 March 2015 Available online 4 April 2015 Keywords: High mobility group box 1 Ischemic heart disease Endothelial cells
We thank Dr Zhu et al. for their interest in our study on the predictive value of increased high mobility group box 1 (HMGB1) levels in patients with chronic heart failure (HF) [1]. We have carefully read with great appreciation Dr Zhu and colleagues' article entitled endothelial cell is critical in HMGB1 mediated cardiac impairment in ischemic heart disease that was recently published in Int J Cardiol [2]. Yes, indeed, our article is just a clinical report without discussing related mechanisms by which increased HMGB1 may predict the fatal outcomes in patients with chronic HF. Because our purpose was only to emphasize the predictive value of HMGB1 in patients with chronic HF other than the underlying mechanisms. However, in frank, our study has one limitation that the study samples we recruited were a little small. Thus, further studies with large sample scales are needed to clarify the accurate predictive value in patients with chronic HF and also its mechanisms by which HMGB1 can take important roles in cardiovascular diseases, especially in chronic HF and in ischemic heart disease. Dr Zhu's group has proposed that endothelial cells may mediate the effect of HMGB1 in ischemic heart disease and has also given the associated reasons. We agree that endothelial cells may, at least in part, take important roles in mediating the myocardial impairment of HMGB1 in ischemic heart disease. However, as to the effects of HMGB1 in ischemic heart disease, lots of studies have been done in recent decades. Recently, we have found that serum levels of HMGB1 were significantly increased in patients with coronary artery disease and correlate with the severity of this disease [3]. Furthermore, we have also found that the myocardial expression of HMGB1 protein was elevated significantly in an acute ⁎ Corresponding author. E-mail address: [email protected] (H.-C. Yao).
http://dx.doi.org/10.1016/j.ijcard.2015.03.380 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
myocardial infarction rat model than in the sham group [4]. These clinical and basic research results suggest that increased HMGB1 was involved in the development and progress of ischemic heart disease. These are in accordance with some recent reported studies [5–7]. Recently, some studies have reported that exogenous HMGB1 protect heart against myocardial infarction [8] or myocardial ischemia reperfusion injury [9]. Thus HMGB1 may be a potential therapeutic target [10] both for basic myocardial ischemia and reperfusion injury research and clinical study in patients with ischemic heart disease. As to the underlying mechanisms that mediating HMGB1 in the impairment or protection in ischemic heart disease is multifactorial. The major mechanisms may involved with endothelial cells [2], PI3K/Akt signal pathway [11], hypoxia inducible factor-1α [12], heat shock protein β1 [13], angiogenesis [14], autophagy [15], nuclear factor kappa B [16] and so on. Although multiple mechanisms are likely involved in HMGB1 mediated pathophysiologic process in ischemic heart disease, further studies should be carried out to better understand the real meaning of HMGB1 in the future. Source of funding This work was supported by the Natural Science Foundation of Shandong Province (ZR2013HL017), the Natural Science Foundation of Liaocheng City (2012NS13), and the Scientific and Technologic Developing Project of Liaocheng City (2014GJH26). Conflict of interest None declared. References [1] T. Liu, Y. Zhang, Y.H. Zhou, Q.F. Han, L.H. Wang, L. Wu, H.C. Yao, Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure, Int. J. Cardiol. 184C (2015) 318–320. [2] Z. Zhu, X. Hu, Z. Fang, S. Zhou, Endothelial cell is critical in HMGB1 mediated cardiac impairment in ischemic heart disease, Int. J. Cardiol. 187 (2015) 39–40. [3] H.C. Yao, A.P. Zhao, Q.F. Han, L. Wu, D.K. Yao, L.X. Wang, Correlation between serum high-mobility group box-1 levels and high-sensitivity C-reactive protein and troponin I in patients with coronary artery disease, Exp. Ther. Med. 6 (2013) 121–124. [4] H.C. Yao, L.J. Yang, Q.F. Han, L.H. Wang, L. Wu, C.Y. Zhang, K.L. Tian, M. Zhang, Postconditioning with simvastatin decreases myocardial injury in rats following acute myocardial ischemia, Exp. Ther. Med. 9 (2015) 1166–1170. [5] X. Hu, X. Zhou, B. He, C. Xu, L. Wu, B. Cui, H. Wen, Z. Lu, H. Jiang, Minocycline protects against myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats, Eur. J. Pharmacol. 638 (2010) 84–89.
R.-J. Gao et al. / International Journal of Cardiology 187 (2015) 434–435 [6] X. Hu, H. Jiang, Q. Bai, X. Zhou, C. Xu, Z. Lu, B. Cui, H. Wen, Increased serum HMGB1 is related to the severity of coronary artery stenosis, Clin. Chim. Acta 406 (2009) 139–142. [7] Y. Lin, L. Chen, W. Li, J. Fang, Role of high-mobility group box-1 in myocardial ischemia/reperfusion injury and the effect of ethyl pyruvate, Exp. Ther. Med. 9 (2015) 1537–1541. [8] X. Zhou, X. Hu, J. Xie, C. Xu, W. Xu, H. Jiang, Exogenous high-mobility group box 1 protein injection improves cardiac function after myocardial infarction: involvement of Wnt signaling activation, J. Biomed. Biotechnol. 2012 (2012) 743879. [9] Y. Zhang, A.X. Zhang, Y.H. Zhou, L.H. Wang, H.C. Yao, Protection of intravenous HMGB1 on myocardial ischemia reperfusion injury, Int. J. Cardiol. 184C (2015) 280–282. [10] X. Hu, W. Fu, H. Jiang, HMGB1: a potential therapeutic target for myocardial ischemia and reperfusion injury, Int. J. Cardiol. 155 (2012) 489. [11] X. Hu, C. Xu, X. Zhou, B. Cui, Z. Lu, H. Jiang, PI3K/Akt signaling pathway involved in cardioprotection of preconditioning with high mobility group box 1 protein during myocardial ischemia and reperfusion, Int. J. Cardiol. 150 (2011) 222–223. [12] H.C. Yao, M. Zhou, Y.H. Zhou, L.H. Wang, D.Y. Zhang, Q.F. Han, T. Liu, L. Wu, K.L. Tian, M. Zhang, Intravenous high mobility group box 1 upregulates HIF-1α expression in
[13]
[14]
[15] [16]
435
ischemic reperfusion myocardium via a protein kinase B-dependent pathway in rats following acute myocardial ischemia, Mol. Med. Rep. (2015) (Accepted, in press). T. Narumi, T. Shishido, Y. Otaki, S. Kadowaki, Y. Honda, A. Funayama, S. Honda, H. Hasegawa, D. Kinoshita, M. Yokoyama, S. Nishiyama, H. Takahashi, T. Arimoto, T. Miyamoto, T. Watanabe, A. Tanaka, C.H. Woo, J.I. Abe, Y. Takeishi, I. Kubota, Highmobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis, J. Mol. Cell. Cardiol. 82 (2015) 11–12. Y. Nakamura, S. Suzuki, T. Shimizu, M. Miyata, T. Shishido, K. Ikeda, S.I. Saitoh, I. Kubota, Y. Takeishi, High mobility group box 1 promotes angiogenesis from bone marrow-derived endothelial progenitor cells after myocardial infarction, J. Atheroscler. Thromb. (Jan 22 2015) (Epub ahead of print). X. Sun, D. Tang, HMGB1-dependent and -independent autophagy, Autophagy 10 (2014) 1873–1876. H. Diao, Z. Kang, F. Han, W. Jiang, Astilbin protects diabetic rat heart against ischemia–reperfusion injury via blockade of HMGB1-dependent NF-κB signaling pathway, Food Chem. Toxicol. 63 (2014) 104–110.