Intracellular MAPK (mitogen-activated protein kinase) signalling cascades probably play an important role in the pathogenesis of cardiac and vascular disease. A substantial amount of basic science research has defined many of the details of MAPK pathway organization and activation, but the role of individual signalling proteins in the pathogenesis of various cardiovascular diseases is still being elucidated. In the present review, the role of the MAPKs ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPK in cardiac hypertrophy, cardiac remodelling after myocardial infarction, atherosclerosis and vascular restenosis will be examined, with attention paid to genetically modified murine model systems and to the use of pharmacological inhibitors of protein kinases. Despite the complexities of this field of research, attractive targets for pharmacological therapy are emerging.

MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets

A review on the medicinal potentials of ginseng and ginsenosides on cardiovascular diseases.

Traditional uses, botany, phytochemistry, pharmacology and toxicology of Panax notoginseng (Burk.) F.H. Chen: A review.

Pharmacological and medical applications of Panax ginseng and ginsenosides: a review for use in cardiovascular diseases.

Cardiovascular Diseases and Panax ginseng: A Review on Molecular Mechanisms and Medical Applications

Total panax notoginsenosides prevent atherosclerosis in apolipoprotein E-knockout mice: Role of downregulation of CD40 and MMP-9 expression

The purpose of this study was to test our hypothesis that p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580 may favorably affect tumor necrosis factor alpha (TNFα) secretion and left ventricular (LV) remodeling after myocardial ischemia (MI) The left anterior descending coronary artery (LAD) was ligated to produce anterior MI in 40 rats that were randomly divided into two groups: p38i group (n = 24) and MIR group (MI rat models, n = 24) A sham operation group without LAD ligation (Sham, n = 16) was also studied SB203580 (2 mg/kg) and saline was injected ip once every 3 days in the first two groups, respectively One and six weeks after MI, cardiac function, myocardial fibrosis, the cardiac expressions of phosphorylated p38 MAPK (p-p38 MAPK), TNFα, alpha smooth muscle actin (αSMA) and collagen I, the ultramicrostructure of the myocardium were examined by echocardiography, histological staining, western blot, immunohistochemical staining, transmission electron microscope (TEM), respectively Treatments with SB203580 suppressed myocardial fibrosis and LV remodeling, as well as attenuated the expressions of p-p38-MAPK, TNFα, αSMA and collagen I as compared with the MIR In conclusion, SB203850 has an effect of inhibiting inflammation-induced fibrosis, which leads to attenuation of LV remodeling

p38 Mitogen-Activated Protein Kinase Inhibition Decreases TNFalpha Secretion and Protects Against Left Ventricular Remodeling in Rats with Myocardial Ischemia

Effect of traditional Chinese medicine Shu-Mai-Tang on attenuating TNFα-induced myocardial fibrosis in myocardial ischemia rats

Effects of Ningdong granule on the dopamine system of Tourette's syndrome rat models

Effect of traditional Chinese medicine Qin-Dan-Jiang-Ya-Tang on remodeled vascular phenotype and osteopontin in spontaneous hypertensive rats.

Fenye Liu

Papers

Total panax notoginsenosides prevent atherosclerosis in apolipoprotein E-knockout mice: Role of downregulation of CD40 and MMP-9 expression

p38 Mitogen-Activated Protein Kinase Inhibition Decreases TNFalpha Secretion and Protects Against Left Ventricular Remodeling in Rats with Myocardial Ischemia

Effect of traditional Chinese medicine Shu-Mai-Tang on attenuating TNFα-induced myocardial fibrosis in myocardial ischemia rats

Effects of Ningdong granule on the dopamine system of Tourette's syndrome rat models

Effect of traditional Chinese medicine Qin-Dan-Jiang-Ya-Tang on remodeled vascular phenotype and osteopontin in spontaneous hypertensive rats.