The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities

Sun, Yu; Wang, Xia; Liu, Tianwei; Zhu, Xiaoyan; Pan, Xudong

doi:10.1186/s13578-022-00815-5

Cited by 42 publications

(75 citation statements)

References 195 publications

(280 reference statements)

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“…Inflammaging is considered a causal risk factor for cardiovascular diseases [ 1 , 2 ]. Throughout life, senescent cells accumulate in vascular tissue, resulting in the development of inflammaging, which consequently leads to cardiovascular diseases [ 1 , 2 , 3 , 4 ]. Senescent cells have been observed in atherosclerotic tissue, and by eliminating senescent cells, the progression of atherosclerosis could be prevented [ 1 , 2 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

“…Senescent cells have been observed in atherosclerotic tissue, and by eliminating senescent cells, the progression of atherosclerosis could be prevented [ 1 , 2 , 5 ]. The abolition of senescent cells has been shown to increase lifespan and provide protection against cardiovascular and age-related diseases in experimental animal studies [ 3 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells

et al. 2023

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Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells

et al. 2023

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“…Instead, extracellular vesicles, such as exosomes, may serve as cell-free therapeutic agents. Not only were they not at risk of promoting tumourigenesis, but they were also less susceptible to immune rejection ( 228 ). An intriguing possibility is that exosomes may carry biological information which may be beneficial or detrimental, suggesting they can function as anti-aging agents ( 229 ).…”

Section: Discussionmentioning

confidence: 99%

Global research trends in atherosclerosis: A bibliometric and visualized study

Tian

Zhang

Wang

et al. 2022

Front. Cardiovasc. Med.

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BackgroundIncreasing evidence has spurred a considerable evolution of concepts related to atherosclerosis, prompting the need to provide a comprehensive view of the growing literature. By retrieving publications in the Web of Science Core Collection (WoSCC) of Clarivate Analytics, we conducted a bibliometric analysis of the scientific literature on atherosclerosis to describe the research landscape.MethodsA search was conducted of the WoSCC for articles and reviews serving exclusively as a source of information on atherosclerosis published between 2012 and 2022. Microsoft Excel 2019 was used to chart the annual productivity of research relevant to atherosclerosis. Through CiteSpace and VOSviewer, the most prolific countries or regions, authors, journals, and resource-, intellectual-, and knowledge-sharing in atherosclerosis research, as well as co-citation analysis of references and keywords, were analyzed.ResultsA total of 20,014 publications were retrieved. In terms of publications, the United States remains the most productive country (6,390, 31,93%). The most publications have been contributed by Johns Hopkins Univ (730, 3.65%). ALVARO ALONSO produced the most published works (171, 0.85%). With a betweenness centrality of 0.17, ERIN D MICHOS was the most influential author. The most prolific journal was identified as Atherosclerosis (893, 4.46%). Circulation received the most co-citations (14,939, 2.79%). Keywords with the ongoing strong citation bursts were “nucleotide-binding oligomerization (NOD), Leucine-rich repeat (LRR)-containing protein (NLRP3) inflammasome,” “short-chain fatty acids (SCFAs),” “exosome,” and “homeostasis,” etc.ConclusionThe research on atherosclerosis is driven mostly by North America and Europe. Intensive research has focused on the link between inflammation and atherosclerosis, as well as its complications. Specifically, the NLRP3 inflammasome, interleukin-1β, gut microbiota and SCFAs, exosome, long non-coding RNAs, autophagy, and cellular senescence were described to be hot issues in the field.

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“…In particular, the Nod-like receptor protein 3 (NLRP3) inflammasome can be primed or indirectly activated by inflammatory cytokines (e.g. IL-1β, IL-6) that are often found as components of the SASP (38,(54)(55)(56).…”

Section: Nlrp3 Caspase-1 and Gasdermin D Mediated Pyroptosis Underlie...mentioning

confidence: 99%

A role for fibroblast-derived SASP factors in the activation of pyroptotic cell death in mammary epithelial cells

Hom

Sun

Campbell

et al. 2023

Preprint

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In normal tissue homeostasis, bidirectional communication between different cell types can shape numerous biological outcomes. Many studies have documented instances of reciprocal communication between fibroblasts and cancer cells that functionally change cancer cell behavior. However, less is known about how these heterotypic interactions shape epithelial cell function in the absence of oncogenic transformation. Furthermore, fibroblasts are prone to undergo senescence, which is typified by an irreversible cell cycle arrest. Senescent fibroblasts are also known to secrete various cytokines into the extracellular space; a phenomenon that is termed the senescence-associated secretory phenotype (SASP). While the role of fibroblast derived SASP factors on cancer cells has been well studied, the impact of these factors on normal epithelial cells remains poorly understood. We discovered that treatment of normal mammary epithelial cells with conditioned media (CM) from senescent fibroblasts (SASP CM) results in a caspase-dependent cell death. This capacity of SASP CM to cause cell death is maintained across multiple senescence-inducing stimuli. However, the activation of oncogenic signaling in mammary epithelial cells mitigates the ability of SASP CM to induce cell death. Despite the reliance of this cell death on caspase activation, we discovered that SASP CM does not cause cell death by the extrinsic or intrinsic apoptotic pathway. Instead, these cells die by an NLRP3, caspase-1, and gasdermin D (GSDMD)-dependent induction of pyroptosis. Taken together, our findings reveal that senescent fibroblasts can cause pyroptosis in neighboring mammary epithelial cells, which has implications for therapeutic strategies that perturb the behavior of senescent cells.

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The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities

Cited by 42 publications

References 195 publications

Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells

Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells

Global research trends in atherosclerosis: A bibliometric and visualized study

A role for fibroblast-derived SASP factors in the activation of pyroptotic cell death in mammary epithelial cells

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