» Articles » PMID: 36555456

Quo Vadis? Immunodynamics of Myeloid Cells After Myocardial Infarction

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2022 Dec 23
PMID 36555456
Authors
Affiliations
Soon will be listed here.
Abstract

Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the "leukocyte supply chain" and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.

Citing Articles

The spleen in ischaemic heart disease.

Heusch G, Kleinbongard P Nat Rev Cardiol. 2025; .

PMID: 39743566 DOI: 10.1038/s41569-024-01114-x.


Advanced Lung Cancer Inflammation Index as Predictor of All-Cause Mortality in ST-Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention.

Trimarchi G, Pizzino F, Lilli A, De Caterina A, Esposito A, Dalmiani S J Clin Med. 2024; 13(20).

PMID: 39458009 PMC: 11508711. DOI: 10.3390/jcm13206059.


Neuroimmune crosstalk : How mental stress fuels vascular inflammation.

Meyer-Lindemann U, Sager H Herz. 2024; 49(4):249-253.

PMID: 38954012 DOI: 10.1007/s00059-024-05254-1.


The Impact of Exercise on Immunity, Metabolism, and Atherosclerosis.

Meyer-Lindemann U, Moggio A, Dutsch A, Kessler T, Sager H Int J Mol Sci. 2023; 24(4).

PMID: 36834808 PMC: 9967592. DOI: 10.3390/ijms24043394.

References
1.
Kacimi R, Karliner J, Koudssi F, Long C . Expression and regulation of adhesion molecules in cardiac cells by cytokines: response to acute hypoxia. Circ Res. 1998; 82(5):576-86. DOI: 10.1161/01.res.82.5.576. View

2.
Schulz R, Heusch G . Tumor necrosis factor-alpha and its receptors 1 and 2: Yin and Yang in myocardial infarction?. Circulation. 2009; 119(10):1355-7. DOI: 10.1161/CIRCULATIONAHA.108.846105. View

3.
Marinkovic G, Grauen Larsen H, Yndigegn T, Szabo I, Mares R, de Camp L . Inhibition of pro-inflammatory myeloid cell responses by short-term S100A9 blockade improves cardiac function after myocardial infarction. Eur Heart J. 2019; 40(32):2713-2723. DOI: 10.1093/eurheartj/ehz461. View

4.
Sandanger O, Ranheim T, Vinge L, Bliksoen M, Alfsnes K, Finsen A . The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury. Cardiovasc Res. 2013; 99(1):164-74. DOI: 10.1093/cvr/cvt091. View

5.
Deniset J, Surewaard B, Lee W, Kubes P . Splenic Ly6G mature and Ly6G immature neutrophils contribute to eradication of . J Exp Med. 2017; 214(5):1333-1350. PMC: 5413339. DOI: 10.1084/jem.20161621. View