Macrophage, a potential targeted therapeutic immune cell for cardiomyopathy
Open accessAbstract
Cardiomyopathy is a major cause of heart failure, leading to systolic and diastolic dysfunction and promoting adverse cardiac remodeling. Macrophages, as key immune cells of the heart, play a crucial role in inflammation and fibrosis. Moreover, exogenous and cardiac resident macrophages are functionally and phenotypically different during cardiac injury. Although experimental evidence has shown that macrophage-targeted therapy is promising in cardiomyopathy, clinical translation remains challenging. In this article, the molecular mechanism of macrophages in cardiomyopathy has been discussed in detail based on existing literature. The issues and considerations of clinical treatment strategies for myocardial fibrosis has also been analyzed.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Standard non-specific immunosuppressive therapies risk silencing reparative macrophage populations.
“Currently, standard non-specific immunosuppressive therapies risk silencing reparative macrophage populations, highlighting the critical need to map specific functional subsets and their spatial niches for precision immunomodulation [3,10,16].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [16]
The Introduction and the section on cardiac remodeling describe reparative macrophages, and the therapeutic-strategy section proposes targeting macrophage phenotypes. But the paper does not say that standard non-specific immunosuppressive therapies risk silencing reparative macrophages; searches for immunosuppressive therapy and steroids did not establish that link. No page numbers were available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Origin and functions of tissue macrophages
Epelman, S., Lavine, K. J., & Randolph, G. J. (2014) · Immunity · doi:10.1016/j.immuni.2014.06.013 · Cited by 1,585 · see citing works
Epelman, S., Lavine, K. J., Beaudin, A. E., Sojka, D. K., Carrero, J. A., Calderon, B., Brija, T., Gautier, E. L., Ivanov, S., Satpathy, A. T., et al. (2014) · Immunity · doi:10.1016/j.immuni.2013.11.019 · Cited by 1,494 · see citing works
Lee, C. G., Homer, R. J., Zhu, Z., Lanone, S., Wang, X., Koteliansky, V., Shipley, J. M., Gotwals, P., Noble, P., Chen, Q., et al. (2001) · The Journal of Experimental Medicine · doi:10.1084/jem.194.6.809 · Cited by 940 · see citing works
Ammirati, E., Frigerio, M., Adler, E. D., Basso, C., Birnie, D. H., Brambatti, M., Friedrich, M. G., Klingel, K., Lehtonen, J., Moslehi, J. J., et al. (2020) · Circulation: Heart Failure · doi:10.1161/circheartfailure.120.007405 · Cited by 811 · see citing works
A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart
Nicolás-Ávila, J. A., Lechuga-Vieco, A. V., Esteban-Martínez, L., Sánchez-Díaz, M., Díaz-García, E., Santiago, D. J., Rubio-Ponce, A., Li, J. L., Balachander, A., Quintana, J. A., et al. (2020) · Cell · doi:10.1016/j.cell.2020.08.031 · Cited by 762 · see citing works
The human heart contains distinct macrophage subsets with divergent origins and functions
Bajpai, G., Schneider, C., Wong, N., Bredemeyer, A., Hulsmans, M., Nahrendorf, M., Epelman, S., Kreisel, D., Liu, Y., Itoh, A., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0059-x · Cited by 712 · see citing works
Hematopoietic Stem Cells Are the Major Source of Multilineage Hematopoiesis in Adult Animals
Sawai, C. M., Babovic, S., Upadhaya, S., Knapp, D. J. H. F., Lavin, Y., Lau, C. M., Goloborodko, A., Feng, J., Fujisaki, J., Ding, L., et al. (2016) · Immunity · doi:10.1016/j.immuni.2016.08.007 · Cited by 381 · see citing works
Flagged first, then by citations
Research works printed but not linked: 82
- Abe H. Takeda N. Isagawa T. Semba H. Nishimura S. Morioka M. S. (2019). Macrophage hypoxia signaling regulates cardiac fibrosis via Oncostatin M. Nat. Commun. 10 (1), 2824. 10.1038/s41467-019-10859-w 31249305 PMC6597788 · DOI
- Aurora A. B. Porrello E. R. Tan W. Mahmoud A. I. Hill J. A. Bassel-Duby R. (2014). Macrophages are required for neonatal heart regeneration. J. Clin. Invest. 124 (3), 1382– 1392. 10.1172/JCI72181 24569380 PMC3938260 · DOI
- Bajpai G. Bredemeyer A. Li W. Zaitsev K. Koenig A. L. Lokshina I. (2019). Tissue resident CCR2- and CCR2+ cardiac macrophages differentially orchestrate monocyte recruitment and fate specification following myocardial injury. Circ. Res. 124 (2), 263– 278. 10.1161/CIRCRESAHA.118.314028 30582448 PMC6626616 · DOI · Paper page
- Barin J. G. Baldeviano G. C. Talor M. V. Wu L. Ong S. Quader F. (2012). Macrophages participate in IL-17-mediated inflammation. Eur. J. Immunol. 42 (3), 726– 736. 10.1002/eji.201141737 22161142 PMC4292791 · DOI · Paper page
- Bezold V. Rosenstock P. Scheffler J. Geyer H. Horstkorte R. Bork K. (2019). Glycation of macrophages induces expression of pro-inflammatory cytokines and reduces phagocytic efficiency. Aging (Albany NY) 11 (14), 5258– 5275. 10.18632/aging.102123 31386629 PMC6682540 · DOI
- Brieler J. Breeden M. A. Tucker J. (2017). Cardiomyopathy: An overview. Am. Fam. Physician 96 (10), 640– 646. 29431384
- Burke M. A. Cook S. A. Seidman J. G. Seidman C. E. (2016). Clinical and mechanistic insights into the genetics of cardiomyopathy. J. Am. Coll. Cardiol. 68 (25), 2871– 2886. 10.1016/j.jacc.2016.08.079 28007147 PMC5843375 · DOI
- Calcagno D. M. Ng R. P. Jr. Toomu A. Zhang C. Huang K. Aguirre A. D. (2020). The myeloid type I interferon response to myocardial infarction begins in bone marrow and is regulated by Nrf2-activated macrophages. Sci. Immunol. 5 (51), eaaz1974. 10.1126/sciimmunol.aaz1974 32978242 PMC7808338 · DOI
- Camelliti P. Borg T. K. Kohl P. (2005). Structural and functional characterisation of cardiac fibroblasts. Cardiovasc. Res. 65 (1), 40– 51. 10.1016/j.cardiores.2004.08.020 15621032 · DOI
- Chatterjee K. Zhang J. Honbo N. Karliner J. S. (2010). Doxorubicin cardiomyopathy. Cardiology 115 (2), 155– 162. 10.1159/000265166 20016174 PMC2848530 · DOI
- Cooper L. T. Jr. (2009). N. Engl. J. Med. 360 (15), 1526– 1538. 10.1056/NEJMra0800028 19357408 PMC5814110 · DOI
- Crespo-Leiro M. G. Metra M. Lund L. H. Milicic D. Costanzo M. R. Filippatos G. (2018). Advanced heart failure: A position statement of the heart failure association of the European society of cardiology. Eur. J. Heart Fail. 20 (11), 1505– 1535. 10.1002/ejhf.1236 29806100 · DOI
- Dick S. A. Macklin J. A. Nejat S. Momen A. Clemente-Casares X. Althagafi M. G. (2019). Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction. Nat. Immunol. 20 (1), 29– 39. 10.1038/s41590-018-0272-2 30538339 PMC6565365 · DOI · Paper page
- Dillmann W. H. (2019). Diabetic cardiomyopathy. Circ. Res. 124 (8), 1160– 1162. 10.1161/CIRCRESAHA.118.314665 30973809 PMC6578576 · DOI
- Duerr G. D. Heinemann J. C. Suchan G. Kolobara E. Wenzel D. Geisen C. (2014). The endocannabinoid-CB2 receptor axis protects the ischemic heart at the early stage of cardiomyopathy. Basic Res. Cardiol. 109 (4), 425. 10.1007/s00395-014-0425-x 24980781 · DOI
- Duncan S. E. Gao S. Sarhene M. Coffie J. W. Linhua D. Bao X. (2020). Macrophage activities in myocardial infarction and heart failure. Cardiol. Res. Pract. 2020, 4375127. 10.1155/2020/4375127 32377427 PMC7193281 · DOI
- Enomoto H. Mittal N. Inomata T. Arimura T. Izumi T. Kimura A. (2021). Dilated cardiomyopathy-linked heat shock protein family D member 1 mutations cause up-regulation of reactive oxygen species and autophagy through mitochondrial dysfunction. Cardiovasc. Res. 117 (4), 1118– 1131. 10.1093/cvr/cvaa158 32520982 · DOI
- Fan D. Takawale A. Lee J. Kassiri Z. (2012). Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease. Fibrogenes. Tissue Repair 5 (1), 15. 10.1186/1755-1536-5-15 PMC3464725 22943504 · DOI · Paper page
- Fan Q. Tao R. Zhang H. Xie H. Lu L. Wang T. (2019). Dectin-1 contributes to myocardial ischemia/reperfusion injury by regulating macrophage polarization and neutrophil infiltration. Circulation 139 (5), 663– 678. 10.1161/CIRCULATIONAHA.118.036044 30586706 · DOI
- Ferrante C. J. Pinhal-Enfield G. Elson G. Cronstein B. N. Hasko G. Outram S. (2013). The adenosine-dependent angiogenic switch of macrophages to an M2-like phenotype is independent of interleukin-4 receptor alpha (IL-4Rα) signaling. Inflammation 36 (4), 921– 931. 10.1007/s10753-013-9621-3 23504259 PMC3710311 · DOI · Paper page
- Frangogiannis N. G. (2019). Cardiac fibrosis: Cell biological mechanisms, molecular pathways and therapeutic opportunities. Mol. Asp. Med. 65, 70– 99. 10.1016/j.mam.2018.07.001 30056242 · DOI
- Garbern J. C. Lee R. T. (2021). Mitochondria and metabolic transitions in cardiomyocytes: Lessons from development for stem cell-derived cardiomyocytes. Stem Cell Res. Ther. 12 (1), 177. 10.1186/s13287-021-02252-6 33712058 PMC7953594 · DOI
- Golovkin A. Kalinina O. Bezrukikh V. Aquino A. Zaikova E. Karonova T. (2021). Imbalanced immune response of T-cell and B-cell subsets in patients with moderate and severe COVID-19. Viruses 13 (10), 1966. 10.3390/v13101966 34696395 PMC8538447 · DOI
- Gombozhapova A. Rogovskaya Y. Shurupov V. Rebenkova M. Kzhyshkowska J. Popov S. V. (2017). Macrophage activation and polarization in post-infarction cardiac remodeling. J. Biomed. Sci. 24 (1), 13. 10.1186/s12929-017-0322-3 28173864 PMC5297120 · DOI
- Hatmal M. M. Alshaer W. Al-Hatamleh M. A. I. Hatmal M. Smadi O. Taha M. O. (2020). Comprehensive structural and molecular comparison of spike proteins of SARS-CoV-2, SARS-CoV and MERS-CoV, and their interactions with ACE2. Cells 9 (12), E2638. 10.3390/cells9122638 33302501 PMC7763676 · DOI
- Heinrichs M. Ashour D. Siegel J. Buchner L. Wedekind G. Heinze K. G. (2021). The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism. Cardiovasc. Res. 117 (13), 2664– 2676. 10.1093/cvr/cvab181 34048536 · DOI
- Hogg C. Horne A. W. Greaves E. (2020). Endometriosis-associated macrophages: Origin, phenotype, and function. Front. Endocrinol. 11, 7. 10.3389/fendo.2020.00007 PMC6989423 32038499 · DOI
- Holscher M. Schafer K. Krull S. Farhat K. Hesse A. Silter M. (2012). Unfavourable consequences of chronic cardiac HIF-1α stabilization. Cardiovasc. Res. 94 (1), 77– 86. 10.1093/cvr/cvs014 22258630 · DOI
- Honold L. Nahrendorf M. (2018). Resident and monocyte-derived macrophages in cardiovascular disease. Circ. Res. 122 (1), 113– 127. 10.1161/CIRCRESAHA.117.311071 29301844 PMC5777215 · DOI
- Hulsmans M. Sager H. B. Roh J. D. Valero-Munoz M. Houstis N. E. Iwamoto Y. (2018). Cardiac macrophages promote diastolic dysfunction. J. Exp. Med. 215 (2), 423– 440. 10.1084/jem.20171274 29339450 PMC5789416 · DOI
- Iannantuoni F. MdM. A. Abad-Jimenez Z. Canet F. Diaz-Pozo P. Lopez-Domenech S. (2020). Mitochondrial alterations and enhanced human leukocyte/endothelial cell interactions in type 1 diabetes. J. Clin. Med. 9 (7), E2155. 10.3390/jcm9072155 32650465 PMC7408780 · DOI
- Ivey M. J. Kuwabara J. T. Pai J. T. Moore R. E. Sun Z. Tallquist M. D. (2018). Resident fibroblast expansion during cardiac growth and remodeling. J. Mol. Cell. Cardiol. 114, 161– 174. 10.1016/j.yjmcc.2017.11.012 29158033 PMC5831691 · DOI · Paper page
- Japp A. G. Gulati A. Cook S. A. Cowie M. R. Prasad S. K. (2016). The diagnosis and evaluation of dilated cardiomyopathy. J. Am. Coll. Cardiol. 67 (25), 2996– 3010. 10.1016/j.jacc.2016.03.590 27339497 · DOI
- Jetten N. Verbruggen S. Gijbels M. J. Post M. J. De Winther M. P. Donners M. M. (2014). Anti-inflammatory M2, but not pro-inflammatory M1 macrophages promote angiogenesis in vivo. Angiogenesis 17 (1), 109– 118. 10.1007/s10456-013-9381-6 24013945 · DOI
- Jum'ah H. Kundrapu S. Jabri A. Kondapaneni M. Tomashefski J. F. Loeffler A. G. (2022). Cardiac macrophage density in covid-19 infection: Relationship to myocyte necrosis and acute lung injury. Cardiovasc. Pathol. 60, 107447. 10.1016/j.carpath.2022.107447 35718082 PMC9212794 · DOI
- Kaczorowski D. J. Nakao A. Vallabhaneni R. Mollen K. P. Sugimoto R. Kohmoto J. (2009). Mechanisms of Toll-like receptor 4 (TLR4)-mediated inflammation after cold ischemia/reperfusion in the heart. Transplantation 87 (10), 1455– 1463. 10.1097/TP.0b013e3181a36e5e 19461481 PMC2766805 · DOI
- Lavine K. J. Epelman S. Uchida K. Weber K. J. Nichols C. G. Schilling J. D. (2014). 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. 111 (45), 16029– 16034. 10.1073/pnas.1406508111 25349429 PMC4234568 · DOI · Paper page
- Lee C. Y. Huang C. H. Rastegari E. Rengganaten V. Liu P. C. Tsai P. H. (2021). Tumor necrosis factor-alpha exacerbates viral entry in SARS-CoV2-infected iPSC-derived cardiomyocytes. Int. J. Mol. Sci. 22 (18), 9869. 10.3390/ijms22189869 34576032 PMC8470197 · DOI
- Li W. Hsiao H. M. Higashikubo R. Saunders B. T. Bharat A. Goldstein D. R. (2016). Heart-resident CCR2(+) macrophages promote neutrophil extravasation through TLR9/MyD88/CXCL5 signaling. JCI Insight 1 (12), 87315. 10.1172/jci.insight.87315 27536731 PMC4985028 · DOI
- Lipshultz S. E. Colan S. D. Gelber R. D. Perez-Atayde A. R. Sallan S. E. Sanders S. P. (1991). Late cardiac effects of doxorubicin therapy for acute lymphoblastic leukemia in childhood. N. Engl. J. Med. 324 (12), 808– 815. 10.1056/NEJM199103213241205 1997853 · DOI
- Luo H. Wong J. Wong B. (2010). Protein degradation systems in viral myocarditis leading to dilated cardiomyopathy. Cardiovasc. Res. 85 (2), 347– 356. 10.1093/cvr/cvp225 19578074 PMC7109953 · DOI
- Martinez F. O. Sica A. Mantovani A. Locati M. (2008). Macrophage activation and polarization. Front. Biosci. 13, 453– 461. 10.2741/2692 17981560 · DOI · Paper page
- McKenna W. J. Maron B. J. Thiene G. (2017). Classification, epidemiology, and global burden of cardiomyopathies. Circ. Res. 121 (7), 722– 730. 10.1161/CIRCRESAHA.117.309711 28912179 · DOI
- Mia M. M. Cibi D. M. Abdul Ghani S. A. B. Song W. Tee N. Ghosh S. (2020). YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction. PLoS Biol. 18 (12), e3000941. 10.1371/journal.pbio.3000941 33264286 PMC7735680 · DOI
- Morano S. Gatti A. Mandosi E. Tiberti C. Fallarino M. Cipriani R. (2007). Circulating monocyte oxidative activity is increased in patients with type 2 diabetes and erectile dysfunction. J. Urol. 177 (2), 655– 659. 10.1016/j.juro.2006.09.046 17222652 · DOI
- Mosser D. M. Edwards J. P. (2008). Exploring the full spectrum of macrophage activation. Nat. Rev. Immunol. 8 (12), 958– 969. 10.1038/nri2448 19029990 PMC2724991 · DOI · Paper page
- Mosser D. M. (2003). The many faces of macrophage activation. J. Leukoc. Biol. 73 (2), 209– 212. 10.1189/jlb.0602325 12554797 · DOI · Paper page
- Mouton A. J. DeLeon-Pennell K. Y. Rivera Gonzalez O. J. Flynn E. R. Freeman T. C. Saucerman J. J. (2018). Mapping macrophage polarization over the myocardial infarction time continuum. Basic Res. Cardiol. 113 (4), 26. 10.1007/s00395-018-0686-x 29868933 PMC5986831 · DOI
- Mukhopadhyay S. Peiser L. Gordon S. (2004). Activation of murine macrophages by Neisseria meningitidis and IFN-gamma in vitro: Distinct roles of class A scavenger and toll-like pattern recognition receptors in selective modulation of surface phenotype. J. Leukoc. Biol. 76 (3), 577– 584. 10.1189/jlb.0104014 15218052 · DOI
- Nahrendorf M. Swirski F. K. Aikawa E. Stangenberg L. Wurdinger T. Figueiredo J. L. (2007). The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J. Exp. Med. 204 (12), 3037– 3047. 10.1084/jem.20070885 18025128 PMC2118517 · DOI · Paper page
- Nishiga M. Wang D. W. Han Y. Lewis D. B. Wu J. C. (2020). COVID-19 and cardiovascular disease: From basic mechanisms to clinical perspectives. Nat. Rev. Cardiol. 17 (9), 543– 558. 10.1038/s41569-020-0413-9 32690910 PMC7370876 · DOI
- O'Rourke S. A. Dunne A. Monaghan M. G. (2019). The role of macrophages in the infarcted myocardium: Orchestrators of ECM remodeling. Front. Cardiovasc. Med. 6, 101. 10.3389/fcvm.2019.00101 31417911 PMC6685361 · DOI
- Peet C. Ivetic A. Bromage D. I. Shah A. M. (2020). Cardiac monocytes and macrophages after myocardial infarction. Cardiovasc. Res. 116 (6), 1101– 1112. 10.1093/cvr/cvz336 31841135 PMC7177720 · DOI
- Perez-Bermejo J. A. Kang S. Rockwood S. J. Simoneau C. R. Joy D. A. Ramadoss G. N. (2020). SARS-CoV-2 infection of human iPSC-derived cardiac cells predicts novel cytopathic features in hearts of COVID-19 patients. New York: bioRxiv. PMC8128284 33723017
- Pollack A. Kontorovich A. R. Fuster V. Dec G. W. (2015). Viral myocarditis--diagnosis, treatment options, and current controversies. Nat. Rev. Cardiol. 12 (11), 670– 680. 10.1038/nrcardio.2015.108 26194549 · DOI · Paper page
- Porter K. E. Turner N. A. (2009). Cardiac fibroblasts: At the heart of myocardial remodeling. Pharmacol. Ther. 123 (2), 255– 278. 10.1016/j.pharmthera.2009.05.002 19460403 · DOI
- Revelo X. S. Parthiban P. Chen C. Barrow F. Fredrickson G. Wang H. (2021). Cardiac resident macrophages prevent fibrosis and stimulate angiogenesis. Circ. Res. 129 (12), 1086– 1101. 10.1161/CIRCRESAHA.121.319737 34645281 PMC8638822 · DOI · Paper page
- Roth G. A. Mensah G. A. Johnson C. O. Addolorato G. Ammirati E. Baddour L. M. (2020). Global burden of cardiovascular diseases and risk factors, 1990-2019: Update from the GBD 2019 study. J. Am. Coll. Cardiol. 76 (25), 2982– 3021. 10.1016/j.jacc.2020.11.010 33309175 PMC7755038 · DOI · Paper page
- Sager H. B. Hulsmans M. Lavine K. J. Moreira M. B. Heidt T. Courties G. (2016). Proliferation and recruitment contribute to myocardial macrophage expansion in chronic heart failure. Circ. Res. 119 (7), 853– 864. 10.1161/CIRCRESAHA.116.309001 27444755 PMC5378496 · DOI
- Shapouri-Moghaddam A. Mohammadian S. Vazini H. Taghadosi M. Esmaeili S. A. Mardani F. (2018). Macrophage plasticity, polarization, and function in health and disease. J. Cell. Physiol. 233 (9), 6425– 6440. 10.1002/jcp.26429 PMC13482560 29319160 · DOI · Paper page
- Sharma A. Garcia G. Arumugaswami V. Svendsen C. N. (2020). Human iPSC-derived cardiomyocytes are susceptible to SARS-CoV-2 infection. New York: bioRxiv. PMC7323681 32835305
- Sierra-Filardi E. Vega M. A. Sanchez-Mateos P. Corbi A. L. Puig-Kroger A. (2010). Heme Oxygenase-1 expression in M-CSF-polarized M2 macrophages contributes to LPS-induced IL-10 release. Immunobiology 215 (9-10), 788– 795. 10.1016/j.imbio.2010.05.020 20580464 · DOI
- Souders C. A. Bowers S. L. Baudino T. A. (2009). Cardiac fibroblast: The renaissance cell. Circ. Res. 105 (12), 1164– 1176. 10.1161/CIRCRESAHA.109.209809 19959782 PMC3345531 · DOI
- Truby L. K. Rogers J. G. (2020). Advanced heart failure: Epidemiology, diagnosis, and therapeutic approaches. JACC. Heart Fail. 8 (7), 523– 536. 10.1016/j.jchf.2020.01.014 32535126 · DOI
- Tsou C. L. Peters W. Si Y. Slaymaker S. Aslanian A. M. Weisberg S. P. (2007). Critical roles for CCR2 and MCP-3 in monocyte mobilization from bone marrow and recruitment to inflammatory sites. J. Clin. Invest. 117 (4), 902– 909. 10.1172/JCI29919 17364026 PMC1810572 · DOI · Paper page
- van Furth R. Cohn Z. A. (1968). The origin and kinetics of mononuclear phagocytes. J. Exp. Med. 128 (3), 415– 435. 10.1084/jem.128.3.415 5666958 PMC2138527 · DOI
- Varol C. Mildner A. Jung S. (2015). Macrophages: Development and tissue specialization. Annu. Rev. Immunol. 33, 643– 675. 10.1146/annurev-immunol-032414-112220 25861979 · DOI · Paper page
- Verma S. K. Garikipati V. N. S. Krishnamurthy P. Schumacher S. M. Grisanti L. A. Cimini M. (2017). Interleukin-10 inhibits bone marrow fibroblast progenitor cell-mediated cardiac fibrosis in pressure-overloaded myocardium. Circulation 136 (10), 940– 953. 10.1161/CIRCULATIONAHA.117.027889 28667100 PMC5736130 · DOI
- Volz H. C. Seidel C. Laohachewin D. Kaya Z. Muller O. J. Pleger S. T. (2010). HMGB1: The missing link between diabetes mellitus and heart failure. Basic Res. Cardiol. 105 (6), 805– 820. 10.1007/s00395-010-0114-3 20703492 · DOI
- Wang M. Qian L. Li J. Ming H. Fang L. Li Y. (2020). GHSR deficiency exacerbates cardiac fibrosis: Role in macrophage inflammasome activation and myofibroblast differentiation. Cardiovasc. Res. 116 (13), 2091– 2102. 10.1093/cvr/cvz318 31790138 · DOI
- Wei Z. Qiao S. Zhao J. Liu Y. Li Q. Wei Z. (2019). miRNA-181a over-expression in mesenchymal stem cell-derived exosomes influenced inflammatory response after myocardial ischemia-reperfusion injury. Life Sci. 232, 116632. 10.1016/j.lfs.2019.116632 31278944 · DOI
- Wu W. Y. Zhou X. J. Sun P. P. Yu X. J. Wang S. X. Qu L. (2020). Interstitial eosinophilic infiltration in diabetic nephropathy is indicative of poor prognosis, with no therapy benefit from steroid. J. Diabetes 12 (12), 881– 894. 10.1111/1753-0407.13077 32506614 · DOI
- Wynn T. A. Chawla A. Pollard J. W. (2013). Macrophage biology in development, homeostasis and disease. Nature 496 (7446), 445– 455. 10.1038/nature12034 23619691 PMC3725458 · DOI · Paper page
- Wynn T. A. Vannella K. M. (2016). Macrophages in tissue repair, regeneration, and fibrosis. Immunity 44 (3), 450– 462. 10.1016/j.immuni.2016.02.015 26982353 PMC4794754 · DOI · Paper page
- Yang L. Han Y. Jaffre F. Nilsson-Payant B. E. Bram Y. Wang P. (2021). An immuno-cardiac model for macrophage-mediated inflammation in COVID-19 hearts. Circ. Res. 129 (1), 33– 46. 10.1161/CIRCRESAHA.121.319060 33853355 PMC8225586 · DOI
- Zaninotto M. Mion M. M. Padoan A. Babuin L. Plebani M. (2020). Cardiac troponin I in SARS-CoV-2-patients: The additional prognostic value of serial monitoring. Clin. Chim. Acta. 511, 75– 80. 10.1016/j.cca.2020.09.036 33010244 PMC7527277 · DOI
- Zhang F. Zhao Q. Jiang Y. Liu N. Liu Q. Shi F. D. (2019). Augmented brain infiltration and activation of leukocytes after cerebral ischemia in type 2 diabetic mice. Front. Immunol. 10, 2392. 10.3389/fimmu.2019.02392 31681285 PMC6797587 · DOI
- Zhang H. Xu A. Sun X. Yang Y. Zhang L. Bai H. (2020). Self-maintenance of cardiac resident reparative macrophages attenuates doxorubicin-induced cardiomyopathy through the SR-A1-c-myc Axis. Circ. Res. 127 (5), 610– 627. 10.1161/CIRCRESAHA.119.316428 32466726 · DOI
- Zhang Z. Tang J. Cui X. Qin B. Zhang J. Zhang L. (2021). New insights and novel therapeutic potentials for macrophages in myocardial infarction. Inflammation 44 (5), 1696– 1712. 10.1007/s10753-021-01467-2 33866463 PMC8460536 · DOI
- Zhao J. Li X. Hu J. Chen F. Qiao S. Sun X. (2019). Mesenchymal stromal cell-derived exosomes attenuate myocardial ischaemia-reperfusion injury through miR-182-regulated macrophage polarization. Cardiovasc. Res. 115 (7), 1205– 1216. 10.1093/cvr/cvz040 30753344 PMC6529919 · DOI
- Zhao J. Lv T. Quan J. Zhao W. Song J. Li Z. (2018). Identification of target genes in cardiomyopathy with fibrosis and cardiac remodeling. J. Biomed. Sci. 25 (1), 63. 10.1186/s12929-018-0459-8 30115125 PMC6094872 · DOI
- Zhou H. Yang J. Zhou C. Chen B. Fang H. Chen S. (2021). A review of SARS-CoV2: Compared with SARS-CoV and MERS-CoV. Front. Med. 8, 628370. 10.3389/fmed.2021.628370 PMC8688360 34950674 · DOI
Cited by
Sorted by citations
Stefanska, M., Kot, M., Koterba, D., & Zeyland, J. (2026) · Cells · doi:10.3390/cells15121110
“Currently, standard non-specific immunosuppressive therapies risk silencing reparative macrophage populations, highlighting the critical need to map specific functional subsets and their spatial niches for precision immunomodulation [3,10,16].”
- Authors
- Chen, G., Jiang, H., Yao, Y., Tao, Z., Chen, W., Huang, F., & Chen, X.
- Affiliations
- Nanjing First Hospital (CN)
- Tongji University (CN)
- Corresponding author
- Huang, Fuhua
- Chen, Xin
- Venue
- Frontiers in Cell and Developmental Biology
- Publisher
- Frontiers Media SA
- Published
- 2022-09-30
- Volume
- 10
- Pages
- 908790-908790
- ISSN
- 2296-634X (ISSN-L)
- PMC
- PMC9561843
- OpenAlex
- W4298144487
- Cited by
- 18
- References
- 7
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 2 · 2022: 1
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81870193)
- Shanghai Pulmonary Hospital
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- macrophages, cardiomyopathy, macrophage-targeted therapy, myocardial fibrosis, cardiac inflammation, cardiac remodeling, heart failure, cardiac resident macrophages, myocardial injury, clinical translation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review