We are analyzing https://link.springer.com/article/10.1007/s12016-025-09025-6.

Title:
Macrophages Unmasked: Their Pivotal Role in Driving Atherosclerosis in Systemic Lupus Erythematosus | Clinical Reviews in Allergy & Immunology
Description:
Systemic lupus erythematosus (SLE) is an autoimmune disease that significantly increases the risk of cardiovascular diseases, particularly atherosclerosis (AS). Understanding the shared pathogenic mechanisms underlying SLE and AS is crucial for developing effective therapeutic strategies. Macrophages, as pivotal immune cells, play a critical role in the initiation and progression of atherosclerotic plaques within the context of SLE. This review delves into the molecular and cellular mechanisms governing macrophage activation and differentiation in response to SLE-related inflammatory mediators, highlighting their roles in lipid metabolism, plaque stability, and immune regulation. Additionally, we discussed the current treatment modalities for SLE and their impact on macrophage functionality, exploring these effects for atherosclerotic progression. By elucidating the intricate relationship between macrophages, SLE pathophysiology, and AS progression, this review underscores the need for a multidisciplinary approach in managing SLE and its cardiovascular complications, aiming to improve patient survival and quality of life through tailored therapeutic interventions addressing both autoimmune and cardiovascular pathologies.
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Keywords {🔍}

pubmed, article, google, scholar, cas, lupus, systemic, erythematosus, central, atherosclerosis, wang, zhang, immunol, chen, macrophage, sle, httpsdoiorgs, liu, macrophages, cells, med, cell, patients, rheumatol, cardiovascular, disease, sci, rev, front, huang, yang, httpsdoiorgfimmu, interferon, res, type, autoimmune, clin, therapeutic, immune, metabolic, syndrome, ann, rheum, analysis, activation, httpsdoiorg, dis, van, endothelial, polarization,

Topics {✒️}

interferon-induced guanylate-binding proteins atm/ampk/mtor signaling pathway month download article/chapter induces exosome-mediated inflammation single-cell sequencing analysis interferon regulates interleukin-1beta hospital-based case-control study reprogramming macrophage-mediated phagocytosis targeting anti-dsdna antibodies immune-mediated inflammatory diseases damage-induced signaling pathways lipid-laden foam cells tlr-mediated syk activation csnk1a1/ck1alpha suppresses autoimmunity single-cell transcriptomic analysis restrain cytokine-mediated autoimmunity anti-c1q autoantibodies van der velden article clinical reviews sle-related inflammatory mediators full article pdf single-cell level high-risk coronary plaque erythrocyte-derived mitochondria interferon-induced polarization cell-mediated activation alleviate inflammation m1 macrophage phenotype modulate antiviral responses improve patient survival modulates plaque composition phase iii trials xiuru guan privacy choices/manage cookies van tiel cm systemic lupus erythematosus hepcidin-ferroportin axis tie2-dependent manner cell prolif e13762 pro-inflammatory state van den bossche single nucleotide polymorphism poor 1-year outcomes low-density lipoprotein van vollenhoven rf van os bw case-control study driving m1 phenotype macrophage-targeted nanomedicine targeted metabolic reprogramming

Questions {❓}

Ganguly D (2018) Do type I interferons link systemic autoimmunities and metabolic syndrome in a pathogenetic continuum?
Hamilton JA, Hsu HC, Mountz JD (2019) Autoreactive B cells in SLE, villains or innocent bystanders?
MacLeod C, Hadoke P, Nixon M (2021) Glucocorticoids: fuelling the fire of atherosclerosis or therapeutic extinguishers?
Walker BR (2006) Cortisol–cause and cure for metabolic syndrome?

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      description:Systemic lupus erythematosus (SLE) is an autoimmune disease that significantly increases the risk of cardiovascular diseases, particularly atherosclerosis (AS). Understanding the shared pathogenic mechanisms underlying SLE and AS is crucial for developing effective therapeutic strategies. Macrophages, as pivotal immune cells, play a critical role in the initiation and progression of atherosclerotic plaques within the context of SLE. This review delves into the molecular and cellular mechanisms governing macrophage activation and differentiation in response to SLE-related inflammatory mediators, highlighting their roles in lipid metabolism, plaque stability, and immune regulation. Additionally, we discussed the current treatment modalities for SLE and their impact on macrophage functionality, exploring these effects for atherosclerotic progression. By elucidating the intricate relationship between macrophages, SLE pathophysiology, and AS progression, this review underscores the need for a multidisciplinary approach in managing SLE and its cardiovascular complications, aiming to improve patient survival and quality of life through tailored therapeutic interventions addressing both autoimmune and cardiovascular pathologies.
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