Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure

By F. Swirski, Matthias Nahrendorf. Science, 2013

1,050 citations recorded by the source corpus.

Cardiovascular diseases claim more lives worldwide than any other. Etiologically, the dominant trajectory involves atherosclerosis, a chronic inflammatory process of lipid-rich lesion growth in the vascular wall that can cause life-threatening myocardial infarction (MI). Those who survive MI can develop congestive heart failure, a chronic condition of inadequate pump activity that is frequently fatal. Leukocytes (white blood cells) are important participants at the various stages of cardiovascular disease progression and complication. This Review will discuss leukocyte function in atherosclerosis, MI, and heart failure.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4cdd76b3d49cc802769db56c7e2fc3c698adc9d4

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Citations in the corpus

Local proliferation dominates lesional macrophage accumulation in atherosclerosis (2013, background): “Its sequence can be summarized as follows: (1) hematopoietic stem cells proliferate in the bone marrow and spleen and give rise to monocytes11,36,37; (2) Monocytes circulate, infiltrate, and differentiate to macrophages5–7,13; (3) Lesional macrophages proliferate and locally augment their numbers in”
Macrophages Facilitate Electrical Conduction in the Heart (2017, neutral): “Cardiac healing after injury requires macrophages (Swirski and Nahrendorf, 2013); however, in contrast to what we know about macrophage function in other organs, specific functions of cardiac macrophages in the steady state are unknown.”
From CRP to IL-6 to IL-1: Moving Upstream To Identify Novel Targets for Atheroprotection (2016, background): “Recent evidence suggests that a wide array of cell types in the monocyte and macrophage lines are involved in atherothrombosis, as are specific cytokines, chemokines, and adhesion molecules that relate to vascular function.(2) Yet, despite accumulating evidence, interest in moving beyond low-density”
Tet2-mediated Clonal Hematopoiesis Accelerates Heart Failure through a Mechanism Involving the IL-1β/NLRP3 Inflammasome (2018, background): “Due to the central role of macrophage activation in post-MI remodeling (31) and the preferential expansion of human TET2-mutant cells into the myeloid lineage in mice (32), we investigated whether the targeted ablation of Tet2 would be sufficient to promote post-MI remodeling.”
Oxidized Low-Density Lipoprotein Induces Long-Term Proinflammatory Cytokine Production and Foam Cell Formation via Epigenetic Reprogramming of Monocytes (2014, background): “It is generally accepted that mononuclear phagocytes play a central role in the various stages of atherosclerosis.(8) The prevailing paradigm has long dictated that monocytes and macrophages do not have any immunologic memory, in contrast to cells of the adaptive immune system.”
Chronic variable stress activates hematopoietic stem cells (2014, neutral): “Inflammatory monocytes and macrophages may lead to plaque rupture, myocardial infarction and stroke 30,31 , and higher blood levels of monocytes and neutrophils correlate with increased mortality 29,32 .”
Macrophage Polarization in Inflammatory Diseases (2014, background): “Monocytes and macrophages play essential roles in the development of atherosclerosis [43].”
Western Diet Triggers NLRP3-Dependent Innate Immune Reprogramming (2018, background): “Notably, blood leukocyte counts and in particular the numbers of circulating monocytes were shown to be tightly associated with hypercholesterolemia and incidence of cardiovascular events (Friedman et al., 1974; Swirski and Nahrendorf, 2013).”
Macrophages are required for neonatal heart regeneration. (2014, neutral): “Conditions that often accompany or precede MI, such as atherosclerosis, obesity, and diabetes, have inflammatory components that disrupt this balance, causing impaired healing (38).”