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
Editorial
. 2019 Jan 18;124(2):183-185.
doi: 10.1161/CIRCRESAHA.118.314357.

The Functional Heterogeneity of Resident Cardiac Macrophages in Myocardial InjuryCCR2+ Cells Promote Inflammation, Whereas CCR2- Cells Protect

Bijun Chen  1 , Adipong Brickshawana  1 , Nikolaos G Frangogiannis  1
Affiliations
Editorial

The Functional Heterogeneity of Resident Cardiac Macrophages in Myocardial InjuryCCR2+ Cells Promote Inflammation, Whereas CCR2- Cells Protect

Bijun Chen et al. Circ Res. .
No abstract available

Keywords: Editorials; chemokines; cytokines; inflammation; macrophages; myocardial infarction.

PubMed Disclaimer

Figures

FIGURE 1:
FIGURE 1:
Contrasting roles of CCR2+ and CCR2− resident cardiac macrophages following cardiac injury. The adult mammalian heart contains both CCR2+ and CCR2− resident macrophages. Cardiomyocyte death releases damage-associated molecular patterns (DAMPs), activating TLR/MyD88-dependent signaling in resident CCR2+ macrophages, and inducing release of cytokines and chemokines. CC chemokines (CC) mediate recruitment of abundant pro-inflammatory CCR2+ monocytes, whereas CXC chemokines (CXC) are implicated in infiltration of neutrophils (which express CXC chemokine receptors/CXCRs). In contrast, CCR2− resident cardiac macrophages appear to have anti-inflammatory actions attenuating infiltration with CCR2+ monocytes. The molecular basis for the anti-inflammatory actions of resident CCR2− macrophages remains unknown. Changes in the profile and relative numbers of resident cardiac macrophage subsets (caused by aging, diabetes, or other pathologic conditions) may have profound effects on the inflammatory and reparative response to myocardial injury. The cartoon was designed using Servier Medical Art (https:smart.servier.com).
See this image and copyright information in PMC

Comment on

References

    1. Pinto AR, Ilinykh A, Ivey MJ, Kuwabara JT, D’Antoni ML, Debuque R, Chandran A, Wang L, Arora K, Rosenthal NA, Tallquist MD. Revisiting Cardiac Cellular Composition. Circ Res 2016; 118:400–409. - PMC - PubMed
    1. Epelman S, Lavine KJ, Beaudin AE, Sojka DK, Carrero JA, Calderon B, Brija T, Gautier EL, Ivanov S, Satpathy AT, Schilling JD, Schwendener R, Sergin I, Razani B, Forsberg EC, Yokoyama WM, Unanue ER, Colonna M, Randolph GJ, Mann DL. Embryonic and Adult-Derived Resident Cardiac Macrophages Are Maintained through Distinct Mechanisms at Steady State and during Inflammation. Immunity 2014; 40:91–104. - PMC - PubMed
    1. Heidt T, Courties G, Dutta P, Sager HB, Sebas M, Iwamoto Y, Sun Y, Da Silva N, Panizzi P, van der Laan AM, Swirski FK, Weissleder R, Nahrendorf M. Differential contribution of monocytes to heart macrophages in steady-state and after myocardial infarction. Circ Res 2014; 115:284–295. - PMC - PubMed
    1. Lavine KJ, Epelman S, Uchida K, Weber KJ, Nichols CG, Schilling JD, Ornitz DM, Randolph GJ, Mann DL. Distinct macrophage lineages contribute to disparate patterns of cardiac recovery and remodeling in the neonatal and adult heart. Proc Natl Acad Sci U S A 2014; 111:16029–16034. - PMC - PubMed
    1. Leid J, Carrelha J, Boukarabila H, Epelman S, Jacobsen SE, Lavine KJ. Primitive Embryonic Macrophages are Required for Coronary Development and Maturation. Circ Res 2016; 118:1498–1511. - PMC - PubMed

Publication types