We are analyzing https://link.springer.com/article/10.1007/s10522-021-09936-9.

Title:
Perspectives on the dynamic implications of cellular senescence and immunosenescence on macrophage aging biology | Biogerontology
Description:
An intricate relationship between impaired immune functions and the age-related accumulation of tissue senescent cells is rapidly emerging. The immune system is unique as it undergoes mutually inclusive and deleterious processes of immunosenescence and cellular senescence with advancing age. While factors inducing immunosenescence and cellular senescence may be shared, however, both these processes are fundamentally different which holistically influence the aging immune system. Our understanding of the biological impact of immunosenescence is relatively well-understood, but such knowledge regarding cellular senescence in immune cells, especially in the innate immune cells such as macrophages, is only beginning to be elucidated. Tissue-resident macrophages are long-lived, and while functioning in tissue-specific and niche-specific microenvironments, senescence in macrophages can be directly influenced by senescent host cells which may impact organismal aging. In addition, evidence of age-associated immunometabolic changes as drivers of altered macrophage phenotype and functions such as inflamm-aging is also emerging. The present review describes the emerging impact of cellular senescence vis-à-vis immunosenescence in aging macrophages, its biological relevance with other senescent non-immune cells, and known immunometabolic regulators. Gaps in our present knowledge, as well as strategies aimed at understanding cellular senescence and its therapeutics in the context of macrophages, have been reviewed.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, aging, senescence, cells, cell, macrophages, cellular, macrophage, senescent, immune, httpsdoiorgs, ageing, immunol, immunosenescence, biol, sharma, nat, mice, human, httpsdoiorgacel, function, agerelated, phenotype, van, wang, httpsdoiorg, age, nature, res, role, system, impact, suppressor, aged, response, polarization, hayflick, springer, impaired, secretory, myeloidderived, disease, rev, stress, sci,

Topics {✒️}

month download article/chapter β-galactosidase-positive macrophage accumulation myeloid-derived suppressor cells sasp-induced macrophage dysfunction pgc-1α/tnfaip3 axis acid microsphere-encapsulated antigen unrepairable double-strand breaks ldl receptor-related protein cell-autonomous tumor suppression interferon-gamma-induced priming pi3k/akt/mtor signalling increases influenza-induced mortality rock-isoform-specific polarization e2f2-deficient macrophages leads age-related macular degeneration nf-κb-dependent mechanism full article pdf hla-e-mediated nk lps-induced macrophage senescence article biogerontology aims age-related inflammatory signatures aged-senescent cells contribute sirt1 regulates macrophage macrophages cross-present poly macrophage-derived il-18 ifn-gamma-dependent transcription effros rb edwards 3rd ck cell cycle arrest humoral immune responses distinct regulatory pathways tissue-resident macrophages targeting senescent cells privacy choices/manage cookies baker dj promote macrophage migration age-related accumulation β-galactosidase mtor immature myeloid cells tissue senescent cells inflammation-mediated degeneration bone marrow article sharma adipose tissue macrophage cd8- dendritic cells resulting macrophage polarization skewed macrophage polarization senescent phenotype induced enhanced oxidative metabolism senescent host cells

Questions {❓}

Aiello A, Farzaneh F, Candore G, Caruso C, Davinelli S, Gambino CM, Ligotti ME, Zareian N, Accardi G (2019) Immunosenescence and its hallmarks: how to oppose aging strategically?
Mevorach D, Trahtemberg U, Krispin A, Attalah M, Zazoun J, Tabib A, Grau A, Verbovetski-Reiner I (2010) What do we mean when we write “senescence,“ “apoptosis,“ “necrosis,“ or “clearance of dying cells”?
Van Beek AA, Van den Bossche J, Mastroberardino PG, de Winther MPJ, Leenen PJM (2019) Metabolic alterations in aging macrophages: ingredients for inflammaging?

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