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RhoA Signaling in Immune Cell Response and Cardiac Disease
被引:11
作者:

Kilian, Lucia Sophie
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机构:
Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany
German Ctr Cardiovasc Res, DZHK, Partner Site Hamburg Kiel Lubeck, D-24105 Kiel, Germany Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany

Frank, Derk
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机构:
Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany
German Ctr Cardiovasc Res, DZHK, Partner Site Hamburg Kiel Lubeck, D-24105 Kiel, Germany Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany

Rangrez, Ashraf Yusuf
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h-index: 0
机构:
Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany
German Ctr Cardiovasc Res, DZHK, Partner Site Hamburg Kiel Lubeck, D-24105 Kiel, Germany
Univ Hosp Heidelberg, Dept Cardiol Angiol & Pneumol, D-69120 Heidelberg, Germany Univ Med Ctr Kiel, Dept Internal Med 3, Cardiol, Angiol,Intens Care, D-24105 Kiel, Germany
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
来源:
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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