Senescence associated macrophages and “macroph-aging”: are they pieces of the same puzzle?

Prattichizzo, Francesco; Bonafè, Massimiliano; Olivieri, Fabiola; Franceschi, Claudio

doi:10.18632/aging.101133

Cited by 60 publications

(52 citation statements)

References 7 publications

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“…However, this approach risks false negatives arising from genuine SNCs that do not express canonical markers, and false positives due to biological use of these proteins outside of senescence. For example, some speculate that macrophages recruited to SNCs as part of immune surveillance make up a large portion of p16 Ink4a -positivity and SA β-gal signal in aged tissue without being senescent per se (174)(175)(176).…”

Section: Discussionmentioning

confidence: 99%

Senescent cells: a therapeutic target for cardiovascular disease

Childs¹,

Hu²,

Deursen³

2018

Journal of Clinical Investigation

151

122

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Cellular senescence, a major tumor-suppressive cell fate, has emerged from humble beginnings as an in vitro phenomenon into recognition as a fundamental mechanism of aging. In the process, senescent cells have attracted attention as a therapeutic target for age-related diseases, including cardiovascular disease (CVD), the leading cause of morbidity and mortality in the elderly. Given the aging global population and the inadequacy of current medical management, attenuating the health care burden of CVD would be transformative to clinical practice. Here, we review the evidence that cellular senescence drives CVD in a bimodal fashion by both priming the aged cardiovascular system for disease and driving established disease forward. Hence, the growing field of senotherapy (neutralizing senescent cells for therapeutic benefit) is poised to contribute to both prevention and treatment of CVD.

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Section: Discussionmentioning

confidence: 99%

Senescent cells: a therapeutic target for cardiovascular disease

Childs¹,

Hu²,

Deursen³

2018

Journal of Clinical Investigation

151

122

View full text Add to dashboard Cite

show abstract

“…Senescence affects most cell types including macrophages, which serve as sentinels against infection (Franceschi et al, 2000). Inflamm-aging has also been designated as macroph-aging, due to the important role played by this cell type in secreting proinflammatory mediators at the local and systemic level (Prattichizzo et al, 2016). Notably, studies of the modulation of circulating monocyte/macrophage polarization during aging suggest different age-related trends for the M2 subset (Costantini et al, 2018).…”

Section: Older Men Show Accelerated Biological Agingmentioning

confidence: 99%

Inflamm-Aging: Why Older Men Are the Most Susceptible to SARS-Cov-2 Complicated Outcomes

Bonafè

Prattichizzo

Giuliani

et al. 2020

Preprint

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that some key features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men. At least four well-recognized aging-related characteristics that are strongly expressed in older men go some way towards explaining why these patients account for the vast majority of fatalities: i. the presence of subclinical systemic inflammation without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation; iii. the downregulation of ACE2 (SARS-CoV-2 receptor), which triggers inflammation, particularly in patients with age-related comorbid diseases such as type II diabetes; and iv. accelerated biological aging, as measured by epigenetic and senescence markers (e.g. telomere shortening) associated to the chronic inflammatory state. Though typical of the aged, especially of elderly men, it is conceivable that these features are also shared by some subsets of the younger population. The high mortality rate of SARS-CoV-2 infection suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection.

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“…With steady accumulation of senescent cells, senescence eventually occurs at the cellular level and then Macrophage senescence is inextricably associated with inflammaging, bridging SASPs and inflammasomes. p16 Ink4a has been implicated in macrophage activation or polarization [29], and SASPs induce senescence-like phenotypes in macrophages [30]. Senescence-related changes in macrophages are speculated to generally represent their proinflammatory activation [31], i.e., proinflammatory effects of macrophages are accompanied by inflammaging to some extent.…”

Section: Macrophage Senescence and Inflammaging: An Intimate Relationmentioning

confidence: 99%

lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases

Nie

Zhang

Wang

et al. 2019

Mediators of Inflammation

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Aging and age-related diseases (ARDs) share basic mechanisms largely involving inflammation. A chronic, low-grade, subclinical inflammation called inflammaging occurs during aging. Autophagy defects, oxidative stresses, senescence-associated secretory phenotypes (SASPs), and DNA damage generally contribute to inflammaging and are largely regulated by numerous lncRNA through two-level vicious cycles disrupting cellular homeostasis: (1) inflammaging and the cellular senescence cascade and (2) autophagy defects, oxidative stress, and the SASP cascade. SASPs and inflammasomes simultaneously cause inflammaging. This review discusses the involvement of macrophage inflammaging in various ARDs and its regulation via lncRNA. Among macrophages, this phenomenon potentially impairs its immunosurveillance and phagocytosis mechanisms, leading to decreased recognition and clearance of malignant and senescent cells. Moreover, SASPs extracellularly manifest to induce paracrine senescence. Macrophage senescence escalates to organ level malfunction, and the organism is more prone to ARDs. By targeting genes and proteins or functioning as competing endogenous RNA (ceRNA), lncRNA regulates different phenomena including inflammaging and ARDs. The detailed mechanism warrants further elucidation to obtain pathological evidence of ARDs and potential treatment approaches.

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Senescence associated macrophages and “macroph-aging”: are they pieces of the same puzzle?

Cited by 60 publications

References 7 publications

Senescent cells: a therapeutic target for cardiovascular disease

Senescent cells: a therapeutic target for cardiovascular disease

Inflamm-Aging: Why Older Men Are the Most Susceptible to SARS-Cov-2 Complicated Outcomes

lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases

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