scholarly journals Role of Higenamine in Heart Diseases: A Mini-Review

2022 ◽  
Vol 12 ◽  
Author(s):  
Jianxia Wen ◽  
Mingjie Li ◽  
Wenwen Zhang ◽  
Haoyu Wang ◽  
Yan Bai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Disease ◽  
Reperfusion Injury ◽  
Cardiac Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

Higenamine, a natural product with multiple targets in heart diseases, is originally derived from Aconitum, which has been traditionally used in China for the treatment of heart disease, including heart failure, arrhythmia, bradycardia, cardiac ischemia/reperfusion injury, cardiac fibrosis, etc. This study is aimed to clarify the role of higenamine in heart diseases. Higenamine has effects on improving energy metabolism of cardiomyocytes, anti-cardiac fibroblast activation, anti-oxidative stress and anti-apoptosis. Accumulating evidence from various studies has shown that higenamine exerts a wide range of cardiovascular pharmacological effects in vivo and in vitro, including alleviating heart failure, reducing cardiac ischemia/reperfusion injury, attenuating pathological cardiac fibrosis and dysfunction. In addition, several clinical studies have reported that higenamine could continuously increase the heart rate levels of healthy volunteers as well as patients with heart disease, but there are variable effects on systolic blood pressure and diastolic blood pressure. Moreover, the heart protection and therapeutic effects of higenamine on heart disease are related to regulating LKB1/AMPKα/Sirt1, mediating the β2-AR/PI3K/AKT cascade, induction of heme oxygenase-1, suppressing TGF-β1/Smad signaling, and targeting ASK1/MAPK (ERK, P38)/NF-kB signaling pathway. However, the interventional effects of higenamine on heart disease and its underlying mechanisms based on experimental studies have not yet been systematically reviewed. This paper reviewed the potential pharmacological mechanisms of higenamine on the prevention, treatment, and diagnosis of heart disease and clarified its clinical applications. The literature shows that higenamine may have a potent effect on complex heart diseases, and proves the profound medicinal value of higenamine in heart disease.

scholarly journals Protective role of melatonin in cardiac ischemia-reperfusion injury: From pathogenesis to targeted therapy

2018 ◽  
Vol 64 (3) ◽  
pp. e12471 ◽  
Author(s):  
Hao Zhou ◽  
Qiang Ma ◽  
Pingjun Zhu ◽  
Jun Ren ◽  
Russel J. Reiter ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Cardiac Ischemia

scholarly journals The protective role of interleukin-18 binding protein in a murine model of cardiac ischemia/reperfusion injury

2015 ◽  
Vol 28 (12) ◽  
pp. 1436-1444 ◽  
Author(s):  
Haifeng Gu ◽  
Minghua Xie ◽  
Liqian Xu ◽  
Xiaojun Zheng ◽  
Yunmei Yang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Murine Model ◽  
Ischemia Reperfusion Injury ◽  
Binding Protein ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Cardiac Ischemia ◽  
Interleukin 18

scholarly journals Mitophagy in Cardiomyocytes and in Platelets: A Major Mechanism of Cardioprotection Against Ischemia/Reperfusion Injury

Physiology ◽  
2018 ◽  
Vol 33 (2) ◽  
pp. 86-98 ◽  
Author(s):  
Weilin Zhang ◽  
Chuyan Chen ◽  
Jun Wang ◽  
Lei Liu ◽  
Yubin He ◽  
...  
Keyword(s):  
Heart Disease ◽  
Reperfusion Injury ◽  
Cellular Response ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Molecular Regulation ◽  
Major Mechanism

Mitophagy, a process that selectively removes damaged organelles by autolysosomal degradation, is an early cellular response to ischemia. Mitophagy is activated in both cardiomyocytes and platelets during ischemia/reperfusion (I/R) and heart disease conditions. We focus on the molecular regulation of mitophagy and highlight the role of mitophagy in cardioprotection.

scholarly journals Role of MnSOD in AIFm2‐Mediated Apoptosis During Cardiac Ischemia/Reperfusion Injury

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Ezar Bess ◽  
Sudha Sharma ◽  
Susmita Bhattarai ◽  
Hosne Ara ◽  
Shenuarin Md. Bhuiyan ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia

Role of Heme Oxygenase-1 in the Regulation of Blood Pressure and Cardiac Function

2003 ◽  
Vol 228 (5) ◽  
pp. 447-453 ◽  
Author(s):  
Yen-Hsu Chen ◽  
Shaw-Fang Yet ◽  
Mark A. Perrella
Keyword(s):  
Blood Pressure ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heme Oxygenase 1 ◽  
Coronary Artery Ligation ◽  
Regulation Of Blood Pressure

Heme oxygenase (HO) is a cytoprotective enzyme that degrades heme (a potent oxidant) to generate carbon monoxide (a vasodilatory gas that has anti-inflammatory properties), bilirubin (an antioxidant derived from biliverdin), and iron (sequestered by ferritin). Because of the properties of inducible HO (HO-1) and its products, we hypothesized that HO-1 would play an important role in the regulation of cardiovascular function. In this article, we will review the role of HO-1 in the regulation of blood pressure and cardiac function and highlight previous studies from our laboratory using gene deletion and gene overexpression transgenic approaches in mice. These studies will include the investigation of HO-1 in the setting of hypertension (renovascular), hypotension (endotoxemia), and ischemia/reperfusion injury (heart). In a chronic renovascular hypertension model, hypertension, cardiac hypertrophy, acute renal failure, and acute mortality induced by one kidney–one clip surgery were more severe in HO-1-null mice. In addition, HO-1-null mice with endotoxemia had earlier resolution of hypotension, yet the mortality and the incidence of end-organ damage were higher in the absence of HO-1. In contrast, mice with cardiac-specific overexpression of HO-1 had an improvement in cardiac function, smaller myocardial infarctions, and reduced inflammatory and oxidative damage after coronary artery ligation and reperfusion. Taken together, these studies suggest that an absence of HO-1 has detrimental consequences, whereas overexpression of HO-1 plays a protective role in hypoperfusion and ischemia/reperfusion injury.

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