Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Sep 2:2019:2164017.
doi: 10.1155/2019/2164017. eCollection 2019.

Role of Inflammatory Cell Subtypes in Heart Failure

Affiliations
Review

Role of Inflammatory Cell Subtypes in Heart Failure

Derek Strassheim et al. J Immunol Res. .

Abstract

Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for heart failure with limited success. A better understanding of the temporal course of the infiltration of the different immune cells and their contribution to the inflammatory process may improve the success for therapy. This brief review outlines the major cell types involved in heart failure, and some of their actions are summarized in the supplementary figure.

PubMed Disclaimer

Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

References

    1. Bond A. R., Iacobazzi D., Abdul-Ghani S., et al. Changes in contractile protein expression are linked to ventricular stiffness in infants with pulmonary hypertension or right ventricular hypertrophy due to congenital heart disease. Open Heart. 2018;5(1, article e000716) doi: 10.1136/openhrt-2017-000716. - DOI - PMC - PubMed
    1. Iacobazzi D., Suleiman M. S., Ghorbel M., George S. J., Caputo M., Tulloh R. M. Cellular and molecular basis of RV hypertrophy in congenital heart disease. Heart. 2016;102(1):12–17. doi: 10.1136/heartjnl-2015-308348. - DOI - PMC - PubMed
    1. Liu T., Song D., Dong J., et al. Current understanding of the pathophysiology of myocardial fibrosis and its quantitative assessment in heart failure. Frontiers in Physiology. 2017;8:p. 238. doi: 10.3389/fphys.2017.00238. - DOI - PMC - PubMed
    1. Vikhorev P. G., Vikhoreva N. N. Cardiomyopathies and related changes in contractility of human heart muscle. International Journal of Molecular Sciences. 2018;19(8, article 2234) doi: 10.3390/ijms19082234. - DOI - PMC - PubMed
    1. Humbert M., Guignabert C., Bonnet S., et al. Pathology and pathobiology of pulmonary hypertension: state of the art and research perspectives. European Respiratory Journal. 2019;53(1, article 1801887) doi: 10.1183/13993003.01887-2018. - DOI - PMC - PubMed