NATURE . COM {
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We are analyzing https://www.nature.com/articles/s41569-023-00957-0.
Title:
Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets | Nature Reviews Cardiology
Description:
Atherosclerosis is a progressive inflammatory disorder of the arterial vessel wall characterized by substantial infiltration of macrophages, which exert both favourable and detrimental functions. Early in atherogenesis, macrophages can clear cytotoxic lipoproteins and dead cells, preventing cytotoxicity. Efferocytosis β the efficient clearance of dead cells by macrophages β is crucial for preventing secondary necrosis and stimulating the release of anti-inflammatory cytokines. In addition, macrophages can promote tissue repair and proliferation of vascular smooth muscle cells, thereby increasing plaque stability. However, advanced atherosclerotic plaques contain large numbers of pro-inflammatory macrophages that secrete matrix-degrading enzymes, induce death in surrounding cells and contribute to plaque destabilization and rupture. Importantly, macrophages in the plaque can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. Regulated necrosis has an important role in the formation and expansion of the necrotic core during plaque progression, and several triggers for necrosis are present within atherosclerotic plaques. This Review focuses on the various forms of programmed macrophage death in atherosclerosis and the pharmacological interventions that target them as a potential means of stabilizing vulnerable plaques and improving the efficacy of currently available anti-atherosclerotic therapies. Macrophages in atherosclerotic plaques can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. In this Review, De Meyer and colleagues describe the various forms of programmed macrophage death in atherosclerosis and the potential therapeutic implications.
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30 years and 10 months (reg. 1994-08-11).
Title:
Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets | Nature Reviews Cardiology
Description:
Atherosclerosis is a progressive inflammatory disorder of the arterial vessel wall characterized by substantial infiltration of macrophages, which exert both favourable and detrimental functions. Early in atherogenesis, macrophages can clear cytotoxic lipoproteins and dead cells, preventing cytotoxicity. Efferocytosis β the efficient clearance of dead cells by macrophages β is crucial for preventing secondary necrosis and stimulating the release of anti-inflammatory cytokines. In addition, macrophages can promote tissue repair and proliferation of vascular smooth muscle cells, thereby increasing plaque stability. However, advanced atherosclerotic plaques contain large numbers of pro-inflammatory macrophages that secrete matrix-degrading enzymes, induce death in surrounding cells and contribute to plaque destabilization and rupture. Importantly, macrophages in the plaque can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. Regulated necrosis has an important role in the formation and expansion of the necrotic core during plaque progression, and several triggers for necrosis are present within atherosclerotic plaques. This Review focuses on the various forms of programmed macrophage death in atherosclerosis and the pharmacological interventions that target them as a potential means of stabilizing vulnerable plaques and improving the efficacy of currently available anti-atherosclerotic therapies. Macrophages in atherosclerotic plaques can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. In this Review, De Meyer and colleagues describe the various forms of programmed macrophage death in atherosclerosis and the potential therapeutic implications.
Website Age:
30 years and 10 months (reg. 1994-08-11).
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conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.comHow Much Does Nature.com Make? {π°}
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Keywords {π}
pubmed, article, google, scholar, cas, atherosclerosis, central, cell, death, biol, atherosclerotic, macrophages, macrophage, nature, mice, plaque, res, thromb, vasc, plaques, arterioscler, ferroptosis, apoptosis, nat, med, pyroptosis, meyer, necrosis, inflammasome, martinet, cells, role, activation, inflammation, human, sci, protein, nlrp, mechanisms, efferocytosis, lipid, cardiol, apolipoprotein, disease, programmed, access, mol, expression, circ, promotes,
Topics {βοΈ}
nature portfolio journals nature portfolio privacy policy high-sensitivity c-reactive protein peroxisome proliferator-activated receptor-Ξ΄ advertising social media caspase-11-gasdermin d-mediated pyroptosis reprints streptozotocin-induced hyperglycemia mediated hypoxia-inducible factor-1Ξ± Ξ²-amyloid precursor protein apolipoprotein e-null mice reduce nf-ΞΊb activation nature+ nature 407 nature 536 nature 464 nature 575 nature secrete matrix-degrading enzymes pfkfb3-targeted pet tracer apolipoprotein e-deficient mice apolipoprotein e-deficient mice simvastatin-dependent plaque stabilization thp-1-derived foam cells pore-forming protein gasdermin p50/p50-mediated suppression publishing agreement annexin-derived peptide ac authors researched data targeted anti-cytokine therapies rip3-mediated macrophage necrosis placebo-controlled study author information authors drug-induced macrophage autophagy apoe3-leiden transgenic mice successful interleukin-1Ξ² inhibition dna-binding cytokine hmgb1 potential ferroptosis-related biomarkers permissions springerlink instant access placebo-controlled clinical trial regulates macrophage retention peer review personal data promotes macrophage necroptosis ripk1 kinase inhibition targeting macrophage necroptosis specific cellular target
Questions {β}
- Apoptosis in atherosclerosis: beneficial or detrimental?
- Drug-induced macrophage autophagy in atherosclerosis: for better or worse?
- Role of autophagy in atherosclerosis: foe or friend?
Schema {πΊοΈ}
WebPage:
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