scholarly journals High mobility group box-1 in hypothalamic paraventricular nuclei attenuates sympathetic tone in rats at post-myocardial infarction

2019 ◽  
Vol 26 (5) ◽  
pp. 555-563 ◽  
Author(s):  
Pang Li ◽  
Yin Jie ◽  
Shi YuGen ◽  
Wang Yu ◽  
Suhua Yan
2019 ◽  
Vol 20 (14) ◽  
pp. 1474-1485 ◽  
Author(s):  
Eyaldeva C. Vijayakumar ◽  
Lokesh Kumar Bhatt ◽  
Kedar S. Prabhavalkar

High mobility group box-1 (HMGB1) mainly belongs to the non-histone DNA-binding protein. It has been studied as a nuclear protein that is present in eukaryotic cells. From the HMG family, HMGB1 protein has been focused particularly for its pivotal role in several pathologies. HMGB-1 is considered as an essential facilitator in diseases such as sepsis, collagen disease, atherosclerosis, cancers, arthritis, acute lung injury, epilepsy, myocardial infarction, and local and systemic inflammation. Modulation of HMGB1 levels in the human body provides a way in the management of these diseases. Various strategies, such as HMGB1-receptor antagonists, inhibitors of its signalling pathway, antibodies, RNA inhibitors, vagus nerve stimulation etc. have been used to inhibit expression, release or activity of HMGB1. This review encompasses the role of HMGB1 in various pathologies and discusses its therapeutic potential in these pathologies.


2017 ◽  
Vol 58 (5) ◽  
pp. 762-768 ◽  
Author(s):  
Rungtiwa Srisuwantha ◽  
Yuka Shiheido ◽  
Norio Aoyama ◽  
Hiroki Sato ◽  
Keitetsu Kure ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tatsuro Kitahara ◽  
Yasuchika Takeishi ◽  
Tetsuro Shishido ◽  
Satoshi Suzuki ◽  
Shigehiko Kato ◽  
...  

High-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein and is released from necrotic cells, inducing inflammatory responses and promoting tissue repair and angiogenesis. To test the hypothesis that HMGB1 enhances angiogenesis and restores cardiac dysfunction after myocardial infarction, we generated transgenic mouse with cardiac specific overexpression of HMGB1 (HMGB1-Tg) using α-myosin heavy chain (MHC) promoter. The left anterior descending coronary artery was ligated in HMGB1-Tg and wild-type littermate (Wt) mice. After coronary artery ligation, HMGB1 was released into circulation from the necrotic cardiomyocytes of HMGB1 overexpressing hearts. The size of myocardial infarction was smaller in HMGB1-Tg than in Wt mice (figure ). Echocardiography and cardiac catheterization demonstrated that cardiac remodeling and dysfunction after myocardial infarction were prevented in HMGB1-Tg mice compared to Wt mice. Furthermore, survival rate after myocardial infarction in HMGB1-Tg mice was higher than that in Wt mice (figure ). Immunohistochemical staining revealed that capillary and arteriole formations after myocardial infarction were enhanced in HMGB1-Tg mice. We demonstrated the first in vivo evidence that HMGB1 enhances angiogenesis, restores cardiac dysfunction, and improves survival after myocardial infarction. These results may provide a novel therapeutic approach for left ventricular dysfunction after myocardial infarction.


2011 ◽  
Vol 4 (3) ◽  
pp. 281-286 ◽  
Author(s):  
Morten V. Sørensen ◽  
Sune Pedersen ◽  
Rasmus Møgelvang ◽  
Jan Skov-Jensen ◽  
Allan Flyvbjerg

2011 ◽  
Vol 17 (2) ◽  
pp. 108-114 ◽  
Author(s):  
Francesco Giallauria ◽  
Plinio Cirillo ◽  
Mariantonietta D’agostino ◽  
Gianluca Petrillo ◽  
Alessandra Vitelli ◽  
...  

2008 ◽  
Vol 80 (1) ◽  
pp. 40-46 ◽  
Author(s):  
T. Kitahara ◽  
Y. Takeishi ◽  
M. Harada ◽  
T. Niizeki ◽  
S. Suzuki ◽  
...  

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