RhoA Signaling in Immune Cell Response and Cardiac Disease

被引:11
作者
Kilian, Lucia Sophie [1 ,2 ]
Frank, Derk [1 ,2 ]
Rangrez, Ashraf Yusuf [1 ,2 ,3 ]
机构
[1] Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany
[2] German Ctr Cardiovasc Res, DZHK, Partner Site Hamburg Kiel Lubeck, D-24105 Kiel, Germany
[3] Univ Hosp Heidelberg, Dept Cardiol Angiol & Pneumol, D-69120 Heidelberg, Germany
关键词
RhoA; cardiac inflammation; immune cells; cardiocrine signaling; cardiac diseases; ATRIAL-NATRIURETIC-PEPTIDE; NUCLEOTIDE EXCHANGE FACTOR; CHRONIC HEART-FAILURE; TUMOR-NECROSIS-FACTOR; TOLL-LIKE RECEPTORS; NEUTROPHIL POLARIZATION; HYPERTROPHIC GROWTH; DENDRITIC CELLS; INNATE IMMUNITY; ACTIVATION;
D O I
10.3390/cells10071681
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chronic inflammation, the activation of immune cells and their cross-talk with cardiomyocytes in the pathogenesis and progression of heart diseases has long been overlooked. However, with the latest research developments, it is increasingly accepted that a vicious cycle exists where cardiomyocytes release cardiocrine signaling molecules that spiral down to immune cell activation and chronic state of low-level inflammation. For example, cardiocrine molecules released from injured or stressed cardiomyocytes can stimulate macrophages, dendritic cells, neutrophils and even T-cells, which then subsequently increase cardiac inflammation by co-stimulation and positive feedback loops. One of the key proteins involved in stress-mediated cardiomyocyte signal transduction is a small GTPase RhoA. Importantly, the regulation of RhoA activation is critical for effective immune cell response and is being considered as one of the potential therapeutic targets in many immune-cell-mediated inflammatory diseases. In this review we provide an update on the role of RhoA at the juncture of immune cell activation, inflammation and cardiac disease.
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页数:15
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