Macrophage death and defective inflammation resolution in atherosclerosis

By I. Tabas. Nature reviews. Immunology, 2009

1,172 citations recorded by the source corpus.

A key event in atherosclerosis is a maladaptive inflammatory response to subendothelial lipoproteins. A crucial aspect of this response is a failure to resolve inflammation, which normally involves the suppression of inflammatory cell influx, effective clearance of apoptotic cells and promotion of inflammatory cell egress. Defects in these processes promote the progression of atherosclerotic lesions into dangerous plaques, which can trigger atherothrombotic vascular disease, the leading cause of death in industrialized societies. In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/721e810dfcbf89b7e4597f9d556912ebc176dc8c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Peter Libby
2. I. Tabas
3. G. Hansson
4. P. Ridker
5. Christian Weber
6. K. Moore
7. Erling Falk
8. J. Bentzon

In Molecular Biology

1. Peter Libby
2. P. Ridker
3. K. Moore
4. Christian Weber
5. G. Hansson
6. Guido Kroemer
7. Linda Partridge
8. Manuel Serrano

Citations in the corpus

• Inflammation and atherosclerosis: signaling pathways and therapeutic intervention (2022, background): “In addition, other potential antigens released from apoptotic cells in the plaques can further promote the progression of the atherosclerotic plaque, and impaired apoptotic cell clearance can sustain atherogenesis.(10) Dysregulation of immune cells in the plaques has been recently uncovered by using”
• Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis (2012, background): “Moreover, boosting autophagy did improve efferocytosis in vitro, which may translate into a beneficial effect in advanced atherosclerosis (Tabas, 2010).”
• Insulin Resistance, Hyperglycemia, and Atherosclerosis (2011, neutral): “…humans support a role for prolonged endoplasmic reticulum (ER) stress in advanced lesional macrophage 578 Cell Metabolism 14, November 2, 2011 ª2011 Elsevier Inc. apoptosis and plaque necrosis, primarily through the action of the ER stress effector C/EBP-homologous protein (CHOP) (Tabas, 2010b).”
• Mechanisms of plaque formation and rupture. (2014, background): “However, when experimentally induced and after necrotic foci have begun to form, macrophage and SMC apoptosis increases necrotic core formation and plaque inflammation,(56,57) possibly because neighboring phagocytes no longer efficiently remove the apoptotic remnants.(36) Instead, they are left to u”
• Progress and challenges in translating the biology of atherosclerosis (2011, background): “The inefficient clearance of dead cells — a process known as efferocytosis — can promote the accumulation of cellular debris and extracellular lipids, forming a lipid-rich pool called the necrotic core of the plaqu”
• The Cellular Biology of Macrophages in Atherosclerosis (2011, positive): “Our increasing understanding of how macrophages die in advanced lesions has provided new targets that could be the basis for drugs that prevent plaque necrosis, particularly inhibitors of proapoptotic ER stress pathways (Tabas, 2010b).”
• The hallmarks of aging. (2013, background): “Likewise, defective inflammatory responses play a critical role in atherosclerosis (Tabas, 2010).”