Lung cancer treatment is evolving, and the role of senescent macrophages in tumor immune evasion has become a key focus. This study explores how senescent macrophages interact with lung cancer cells, contributing to tumor progression and immune dysfunction. As aging impairs macrophage functions, including phagocytosis and metabolic signaling, it promotes chronic inflammation and cancer development. p16-positive macrophages are common in aged mice, and their clearance slows tumor growth, suggesting these cells support tumor proliferation and immune evasion. Targeting the senescence-associated secretory phenotype (SASP) and reprogramming senescent macrophages offers potential therapeutic benefits, including reversing immune aging and boosting anti-tumor immunity. However, translating these findings into clinical practice requires further molecular understanding and rigorous clinical trials.
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http://dx.doi.org/10.14336/AD.2024.1404 | DOI Listing |
Lung cancer treatment is evolving, and the role of senescent macrophages in tumor immune evasion has become a key focus. This study explores how senescent macrophages interact with lung cancer cells, contributing to tumor progression and immune dysfunction. As aging impairs macrophage functions, including phagocytosis and metabolic signaling, it promotes chronic inflammation and cancer development.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Boston Children's Hospital, Boston, MA, USA.
Background: Alzheimer's disease (AD), an age-associated neurodegenerative disorder, is characterized by progressive neuronal loss and the accumulation of misfolded proteins such as amyloid-β and tau. While neuroinflammation, mediated by microglia and brain-resident macrophages, plays a pivotal role in AD pathogenesis, the intricate interactions among age, genes, and other risk factors remain elusive. Somatic mutations, known to accumulate with age, instigate clonal expansion across diverse cell types, impacting both cancer and non-cancerous conditions.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Aging microglia accumulate lipid droplets (LDs), secrete pro-inflammatory cytokines, and are defective in phagocytosis. The E4 allele of Apolipoprotein E (APOE) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) and is associated with increased neuroinflammation and LD accumulation. Here, we aimed to determine if the effects of aging and the E4 allele are synergistic in causing the accumulation of LDs seen in LOAD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky/Sanders-Brown Center on Aging, Lexington, KY, USA.
Background: The characterization of intercellular communication between peripheral immune cells and the central nervous system (CNS) are essential for understanding the brain's response to aging and disease states, such as Alzheimer's disease. MicroRNAs (miRNAs) constitute a class of small non-coding RNAs that play a crucial role in regulating various biological and pathological processes, including those related to immunity and inflammation. MiR-223-3p, residing on the X chromosome, is a pivotal miRNA involved in the inflammatory response, with its expression being enriched in macrophages/microglia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Washington University in St. Louis, School of Medicine, St. Louis, MO, USA.
Therapeutics against targets supported by human genetics are more than twice as likely to make it to the clinic as an FDA approved drug. In 2012 the National Institute on Aging in response to the U.S.
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