Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases

Song, Ping; An, Junqing

doi:10.3390/cells9030671

Cited by 127 publications

(129 citation statements)

References 163 publications

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“…The notion that cellular senescence is an imperceptible underlying force in the pathogenesis of wound chronicity and ulcers recurrence has been accrued for years (45)(46)(47)(48). Consequently, we suggest that diabetes-associated wound healing failure and reduced tissue resilience are clinical translations of an "entrenched" wound senescent cells society, with self-perpetuating and propagating abilities.…”

Section: Introductionmentioning

confidence: 84%

Cellular Senescence as the Pathogenic Hub of Diabetes-Related Wound Chronicity

et al. 2020

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Diabetes is constantly increasing at a rate that outpaces genetic variation and approaches to pandemic magnitude. Skin cells physiology and the cutaneous healing response are progressively undermined in diabetes which predisposes to lower limb ulceration, recidivism, and subsequent lower extremities amputation as a frightened complication. The molecular operators whereby diabetes reduces tissues resilience and hampers the repair mechanisms remain elusive. We have accrued the notion that diabetic environment embraces preconditioning factors that definitively propel premature cellular senescence, and that ulcer cells senescence impair the healing response. Hyperglycemia/oxidative stress/mitochondrial and DNA damage may act as major drivers sculpturing the senescent phenotype. We review here historical and recent evidences that substantiate the hypothesis that diabetic foot ulcers healing trajectory, is definitively impinged by a self-expanding and self-perpetuative senescent cells society that drives wound chronicity. This society may be fostered by a diabetic archetypal secretome that induces replicative senescence in dermal fibroblasts, endothelial cells, and keratinocytes. Mesenchymal stem cells are also susceptible to major diabetic senescence drivers, which accounts for the inability of these cells to appropriately assist in diabetics wound healing. Thus, the use of autologous stem cells has not translated in significant clinical outcomes. Novel and multifaceted therapeutic approaches are required to pharmacologically mitigate the diabetic cellular senescence operators and reduce the secondary multi-organs complications. The senescent cells society and its adjunctive secretome could be an ideal local target to manipulate diabetic ulcers and prevent wound chronification and acute recidivism. This futuristic goal demands harnessing the diabetic wound chronicity epigenomic signature.

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Section: Introductionmentioning

confidence: 84%

Cellular Senescence as the Pathogenic Hub of Diabetes-Related Wound Chronicity

et al. 2020

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“…It is important to emphasize here that senescent cells (HPFs and HDFs) are one of the most widely used models for studying inflammatory processes. Accumulation of senescent cells in an organism leads to disruption of tissues and cellular structure and function [72]. The phenomenon of cellular senescence has been demonstrated to play a causal role in driving ageing [72] and chronic diseases [7,9,72].…”

Section: Discussionmentioning

confidence: 99%

“…Accumulation of senescent cells in an organism leads to disruption of tissues and cellular structure and function [72]. The phenomenon of cellular senescence has been demonstrated to play a causal role in driving ageing [72] and chronic diseases [7,9,72]. Namely, the above-mentioned cells are accepted models [7,9] used to investigate the effect of plant extracts and pure compounds on inflammation.…”

Section: Discussionmentioning

confidence: 99%

Medicinal Properties of Lilium candidum L. and Its Phytochemicals

Zaccai

Yarmolinsky²,

Khalfin

et al. 2020

Plants

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Lilium candidum L., known as Madonna, meadow, or white lily, is a bulbous plant from the Liliaceae family, originating in the Middle East. L. candidum has been abundantly used in folk medicine since ancient times to relieve a variety of ailments, including age-related diseases, burns, ulcers, and coughs. The aim of this article is to investigate the anti-inflammatory and anti-diabetic activities of L. candidum extracts and its active phytochemicals. Some active volatile phytochemicals were identified using gas chromatography–mass spectrometry (GC-MS) analysis. Significant (p < 0.001) anti-diabetic properties of the extracts kaempferol, linalool, citronellal, and humulene were demonstrated by an elevation in glucose uptake by adipocytes. The significant (p < 0.01) effect of the plant extracts kaempferol, citronellal, and humulene on the secretion of pro-inflammatory cytokines interleukin 6 (IL-6) and interleukin 8 (IL-8) was demonstrated using enzyme-linked immunosorbent assay. Altogether, L. candidum and its rich collection of phytochemicals hold promising medicinal potential, and further investigations of its therapeutic prospects are encouraged.

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“…Due to their resistance to apoptosis [ 66 ], senescent cells persist in tissues and they can promote a negative impact on their environment through various mechanisms. First, as mentioned above, senescent cells become proinflammatory foci scattered throughout tissues promoting immune cell infiltration that results in collateral tissue damage over time [ 67 , 68 ]. Besides the exacerbation of local inflammation, senescent cells also constitute an important source of factors that contribute to age-related systemic chronic inflammation [ 69 ].…”

Section: Cellular Senescencementioning

confidence: 99%

Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?

Aquino-Martínez

Khosla

Farr

et al. 2020

IJMS

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The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction.

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Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases

Cited by 127 publications

References 163 publications

Cellular Senescence as the Pathogenic Hub of Diabetes-Related Wound Chronicity

Cellular Senescence as the Pathogenic Hub of Diabetes-Related Wound Chronicity

Medicinal Properties of Lilium candidum L. and Its Phytochemicals

Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?

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