Senescent intimal foam cells are deleterious at all stages of atherosclerosis
Open accessAbstract
Wreaking havoc while (growth-)arrested: Cells enter a state of senescence in response to certain stresses. Studying mouse models, Childs et al. examined the role of senescent lipid-loaded macrophages (so-called “foam cells”) in the pathogenesis of atherosclerosis. At early stages of atherosclerosis, senescent foam cells promoted the expression of inflammatory cytokines. At later stages, they promoted the expression of matrix metalloproteases implicated in the rupture of atherosclerotic plaque, which can lead to blood clots. Experimental removal of the senescent cells had beneficial effects at both stages of the disease. Science , this issue p. 472
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Genetic removal of senescent cells in mouse models improves several age-related conditions, including vascular reactivity, atherosclerotic plaques, pulmonary function, osteoarthritis, fatty liver disease, pulmonary fibrosis, and bone loss.
“Clearance of Sncs in INK-ATTAC or p16-3MR mice restores vascular reactivity (12), stabilizes atherosclerotic plaques (13), improves pulmonary function (14), alleviates osteoarthritis (10), improves fatty liver disease (15), improves lung function in a pulmonary fibrosis model (14), and prevents age-related bone loss (16).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [13]
For citation (13), the paper reports that clearing senescent cells in mice improved fibrous-cap thickness, collagen content, and other surrogate markers of plaque stability (section labeled Abstract; page not provided). It concludes that these results strongly suggest greater plaque stability, but it does not establish plaque stabilization through observed rupture outcomes. The other conditions in the sentence are attached to different citations and are not assessed here. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAtherosclerotic plaques in LDL receptor-null mice accumulate high amounts of SA-β-Gal and p16-positive endothelial cells, vascular smooth muscle cells and macrophages.
“Recently, atherosclerotic plaques from LDL receptor-null mice were found to accumulate high amounts of SA-β-Gal and p16-positive endothelial cells, vascular smooth muscle cells and macrophages.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [175]
The paper reports SA β-Gal–positive lesions and elevated p16Ink4a transcripts in plaque-rich aortic arches of Ldlr−/− mice. Its plaque microscopy passage (Fig. 1A; page unavailable) identifies three senescent cell types resembling endothelial cells, VSMCs, and macrophages, but explicitly says their origins cannot be accurately determined. The claim overstates those cell identities as definitive. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAge-related changes in murine liver cells include increased SA-β-gal activity, DNA damage, TAFs, karyomegaly, SADS, ALISE, LINE-1 elements, and SASP factors, some specified to occur in hepatocytes.
“Age-related changes in murine liver cells include increased SA-β-gal activity78, DNA damage, TAFs19,20,78, karyomegaly, SADS26, ALISE26, LINE-1 elements79, and SASP factors40, some of them specified to occur in hepatocytes19,26.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [20]
The passage on plaque-rich aortic arches (section labeled Abstract; page unavailable) reports elevated SASP components in mice, supporting the SASP-factors portion attached to this citation. It concerns atherosclerotic tissue, not age-related changes in murine liver cells or hepatocytes; the other listed markers are attached to different citations. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSenescence-associated markers have been identified in atherosclerosis, abdominal aortic aneurysm, and thoracic aortic aneurysm in human and mouse models.
“Senescence-associated markers have also been identified in the context of vascular diseases such as atherosclerosis and abdominal aortic aneurysm and thoracic aortic aneurysm in both human and mouse models69–72.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [71]
The paper reports senescence-associated findings in atherosclerosis: its Abstract section describes shortened telomeres in human plaques, and the mouse experiments identify SA β-Gal activity and elevated senescence-marker transcripts in lesions. Our copy does not report such markers in abdominal or thoracic aortic aneurysms. No page number is available for these passages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSenescent cells accumulate with ageing and age-associated diseases, limiting lifespan and healthspan in mice.
“Senescent cells accumulate with ageing and age-associated diseases, limiting lifespan and healthspan in mice11–16.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [14]
The paper reports that senescent cells accumulate in atherosclerotic lesions in mice and contribute to disease progression (Abstract; page unavailable). It does not establish accumulation with ageing generally or show that senescent cells limit mouse lifespan or healthspan. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Cellular senescence encompasses heterogeneous cellular states triggered by prolonged cell stress resulting in irreversible arrest of proliferation and permanent changes to cell function in vivo.
“Cellular senescence, a central hallmark of aging,13,14 encompasses heterogeneous cellular states triggered by prolonged cell stress resulting in the irreversible arrest of proliferation and permanent changes to cell function in vivo.15,16,17,18,19”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [16]
The passage labeled Abstract describes senescence as a stress response involving permanent growth arrest and secretion of biologically active molecules; it also reports three morphologically distinct senescent cell types in advanced plaques. It does not specify that the stress must be prolonged or that the changes to cell function are permanent, so those parts of the broader definition are not established by this paper. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn aged organisms, senescent cells can contribute to a variety of age-related pathologies, including pulmonary fibrosis, biliary liver damage, arteriosclerosis, retinopathy, osteoarthritis, dementia and diabetes mellitus.
“In aged organisms, senescent cells can contribute to a variety of age- related pathologies, including pulmonary fibrosis, biliary liver damage, arteriosclerosis, retinopathy, osteoarthritis, dementia and diabetes mellitus 13-19 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [14]
The paper’s Abstract reports that senescent cells drive atherosclerosis in susceptible mice, supporting the arteriosclerosis example. It does not address the other listed pathologies or establish the claim specifically for aged organisms. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescent cells contribute to the initiation and progression of various aging-related chronic diseases.
“and contribute to the initiation and progression of various aging-related chronic diseases.9,10,11”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [9]
The Abstract reports that senescent cells drive the onset and progression of atherosclerosis in a mouse model. It does not establish their role in the initiation and progression of various aging-related chronic diseases; that broader claim goes beyond this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescent cell clearance alleviates plaque formation and disease progression.
“alleviated plaque formation and disease progression46,118”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [118]
It cannot be excluded that the beneficial effects of senolysis in atherosclerosis-prone mice result from eliminating inflammatory macrophages.
“it cannot be ruled out that the positive effects of senolysis in atherosclerosis-prone mice175 are the consequence of elimination of inflammatory macrophages.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [175]
Removing p16-positive cells in p16-3MR and INK-ATTAC transgenic mice by genetic methods or senolytics reduces plaque formation and progression and dampens the SASP.
“Removal of p16-positive cells in both p16-3MR and INK-ATTAC transgenic mice by both genetic methods and senolytics reduced plaque formation and progression, while dampening the SASP175.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [175]
The INK-ATTAC and p16-3MR mouse models have substantially advanced knowledge about whether senescent cells contribute to ageing and age-related diseases in model organisms, covering conditions such as Parkinson disease, Alzheimer disease, atherosclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and osteoarthritis.
“These two mouse models have greatly accelerated our understanding of whether senescent cells contribute to ageing and age-related diseases, at least in model organisms, for numerous diseases, including Parkinson disease196, Alzheimer disease197,198, atherosclerosis175, idiopathic pulmonary fibrosis199, chronic obstructive pulmonary disease200 and osteoarthritis201.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [175]
Lipid-laden foamy macrophages in atherosclerosis have a senescent phenotype and are drivers of pathology.
“lipid-laden ‘foamy macrophages’ in atherosclerosis which have a senescent phenotype and are drivers of pathology37.”
From APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia (2024) · cites this paper as [37]
Telomeric DNA damage and attrition lead to DNA damage response foci that colocalize with telomeric sequences, known as telomere-associated foci or telomere-induced foci.
“Telomeric DNA damage and attrition leads to DDR foci colocalizing with telomeric sequences known as telomere-associated foci (TAF) or telomere-induced foci (TIF)19,20.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [20]
The Abstract says that human plaques contain cells with shortened telomeres, but it does not describe DNA damage response foci colocalizing with telomeric sequences. Searches for telomere-associated foci, telomere-induced foci, and telomeric DNA damage found no passage in our copy addressing that claim. (LLM, conf=0.73)
Experimental — accuracy not yet measuredLipid droplets have not been studied functionally in brain myeloid cells in humans or vertebrates, and less than a handful of papers report the histological presence of lipid droplets in human brains.
“Surprisingly, lipid droplets have not been studied functionally in brain myeloid cells in humans or vertebrates, and less than a handful of papers report the histological presence of lipid droplets in human brains11,12.”
From Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain (2020) · cites this paper as [11]
The passages on atherosclerotic plaques (section labeled Abstract; page unavailable) describe lipid-loaded macrophage-like cells in mouse arteries, not brain myeloid cells. Searches for brain microglia, lipid droplets, and human-brain histology found no passage addressing whether functional studies exist or how many papers report their histological presence. (LLM, conf=0.76)
Experimental — accuracy not yet measuredSenolytic agents that selectively eliminate senescent cells confirm that senescent cells contribute to ageing in atherosclerotic plaques and osteoarthritic lesions.
“Application of ‘senolytic’ agents that selectively eliminate senescent cells confirm that they contribute to ageing e.g. in atherosclerotic plaques66 and osteoarthritic lesions67.”
From The central role of DNA damage in the ageing process (2021) · cites this paper as [66]
Via the SASP, senescent cells contribute to multiple chronic health conditions associated with inflammaging, including atherosclerosis, osteoarthritis, cancer, myeloid skewing in the bone marrow, pulmonary fibrosis, Alzheimer's disease, Parkinson's disease, and insulin resistance.
“Via the SASP, senescent cells contribute to multiple chronic health conditions associated with inflammaging, e.g., atherosclerosis (16), osteoarthritis (17), cancer (18), myeloid skewing in the bone marrow (19), pulmonary fibrosis (20), Alzheimer’s disease and Parkinson’s disease (21–23), and insulin resistance (24).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [16]
Senescence occurs at sites of atherosclerotic plaques, where it participates in multiple stages of atherogenesis and, through a paracrine SASP mechanism, accelerates the atherosclerotic process.
“Additionally, senescence occurs at sites of atherosclerotic plaques, where it participates in multiple stages of atherogenesis (16, 39) and, through a paracrine SASP mechanism, accelerates the atherosclerotic process.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [16]
Several senolytics reduce or improve inflammatory or age-related phenotypes in preclinical models, specifically atherosclerosis (D+Q, navitoclax), osteoarthritis (navitoclax), idiopathic pulmonary fibrosis (D+Q), and insulin resistance, as well as rejuvenating hematopoietic stem cells in aged mice (navitoclax).
“Several senolytics reduce or improve inflammatory or age-related phenotypes in preclinical models, specifically atherosclerosis (D+Q, navitoclax) (16, 41), osteoarthritis (navitoclax) (17), idiopathic pulmonary fibrosis (D+Q), and insulin resistance (23), among others, as well as rejuvenating hematopoietic stem cells in aged mice (navitoclax) (19).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [16]
Navitoclax clears senescent cells appearing in early atherosclerotic plaques and after sublethal irradiation in skeletal muscle and bone marrow.
“Navitoclax treatment has been shown to eliminate senescent cells that arise in early atherosclerotic plaques (30) and upon sublethal irradiation in both skeletal muscle and the bone marrow (93).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [30]
These models have greatly sped up knowledge about how senescent cells contribute to age-related changes and diseases such as osteoarthritis and atherosclerosis.
“Use of these models has dramatically accelerated our understanding of the contribution of senescent cells to various age-associated alterations and pathologies, including osteoarthritis and atherosclerosis (30,31).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [30]
Senescent cells participate in starting and maturing atheromas in atherosclerosis.
“In atherosclerosis, senescent cells contribute atheroma initiation and maturation, and navitoclax administration reduces plaque burden (30).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [30]
In mice, removing senescent cells genetically or with senolytics has generally helped across many diseases and conditions.
“Using mouse models, elimination of these cells, through either genetic means or senolytic therapies, has largely shown beneficial impacts, irrespective of the disease or condition investigated (29-31, 99, 100).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [30]
Navitoclax administration reduces plaque burden in atherosclerosis.
“In atherosclerosis, senescent cells contribute atheroma initiation and maturation, and navitoclax administration reduces plaque burden (30).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [30]
The SASP is a protracted and chronic source of inflammatory and other plaque-destabilizing factors, gradually contributing to atherosclerosis pathogenesis.
“Emerging experimental evidence indicates that, in contrast to an acute inflammatory response, the SASP is a protracted and chronic source of inflammatory and other plaque-destabilizing factors,9,10 gradually contributing to atherosclerosis pathogenesis.”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Cellular senescence is accompanied by a pro-inflammatory phenotype known as the senescence-associated secretory phenotype (SASP), which produces pro-inflammatory cytokines, metalloproteinases, and other factors.
“Cellular senescence is defined as an irreversible cell cycle arrest (mechanism outlined in Figure 1)8 and is accompanied by a pro-inflammatory phenotype. The phenotype is referred to as the senescence-associated secretory phenotype (SASP), producing pro-inflammatory cytokines [interleukin (IL)-1α, IL-1β, IL-6, IL-8, IL-18, CCL-2, tumour necrosis factor α (TNF-α)], metalloproteinases (MMP-1, -2, -3”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Cellular senescence is observed in early stages of atherosclerosis, affecting different cell types in the arterial wall.
“Cellular senescence is observed in early stages of atherosclerosis,9 affecting different cell types in the arterial wall that have distinct roles in the pathogenesis of this disease: endothelial cells (ECs),96–98 vascular smooth muscle cells (VSMCs),45,99–101 macrophages, foam cells,9,102 monocytes,103 fibroblasts,104–106 and T cells.107,108”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Navitoclax, a Bcl-2 inhibitor, has beneficial effects in atherosclerosis and may be a good candidate for targeting T-EMRA cells, which overexpress Bcl-2 family proteins.
“Navitoclax, a Bcl-2 inhibitor, has beneficial effects in atherosclerosis,9 and may be a good candidate for the targeting of T-EMRA cells, which overexpress Bcl-2 family proteins.116”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Senescent cell elimination diminished plaque size, inflammation, and instability features.
“Senescent cell elimination diminished plaque size, inflammation, and instability features.9”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
The positive effect of senescent cell removal in atherosclerosis in LDL receptor-knockout mice has been replicated in INK-ATTACK, p16-3MR, and INK-nitroreductase mouse models using the senolytic navitoclax.
“The positive effect of senescent cell removal in atherosclerosis in LDL receptor-knockout mice has been replicated in INK-ATTACK, p16-3MR, and INK-nitroreductase mouse models using the senolytic navitoclax (ABT-263).9”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Cellular senescence promotes atherosclerosis in each developmental phase.
“On the other hand, cellular senescence promotes atherosclerosis in each developmental phase.9,101”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Selective removal of p16 INK4a-positive senescent cells prevented atherosclerosis, stabilized plaques, and decreased plaque inflammation.
“Selective removal of p16 INK4a-positive senescent cells prevented atherosclerosis, while stabilizing plaques and decreasing plaque inflammation.9”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [9]
Matrix metalloproteinase secretion from foamy macrophages triggers plaque degradation.
“Matrix metalloproteinase secretion from these cells also trigger plaque degradation (Childs et al, 2016).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Childs et al, 2016
Uncleared senescent cells accumulate during aging and disease, and generate chronic inflammation that could worsen outcome and/or drive atherosclerosis.
“However, uncleared senescent cells accumulate during aging and disease (perhaps due to a dysfunctional immune system or a suppressive milieu), and these generate chronic inflammation that could worsen outcome and/or drive atherosclerosis 84 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [84]
Senescent cells appeared within 9 days of fat feeding, and both genetic and pharmacological elimination of p16 positive cells reduced plaque formation and progression.
“Senescent cells appeared within 9 days of fat feeding, and both genetic and pharmacological elimination of p16 positive cells reduced plaque formation and progression 84 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [84]
A recent study utilised electron microscopy to identify crystals proposed to be the product of X-Gal cleavage by SAβG.
“In contrast, an intriguing recent study utilised electron microscopy to identify crystals proposed to be the product of X-Gal cleavage by SAβG 84 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [84]
This study reported more than 50% of all plaque cells to be senescent, including VSMCs, macrophages and endothelial cells.
“This study reported more than 50% of all plaque cells to be senescent, including VSMCs, macrophages and endothelial cells 84 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [84]
Elimination of senescent cells has proven to be an effective strategy in improving a number of age-related diseases.
“Elimination of senescent cells has proven to be an effective strategy in improving a number of age-related diseases (Childs et al., 2016; Ogrodnik et al., 2017; Schafer et al., 2017; Xu et al., 2018).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Childs et al., 2016
Genetic elimination of p16-positive senescent cells ameliorated atherosclerosis and osteoarthritis in mice.
“Further highlighting the potential of targeting senescence as a way to counteract age-related diseases, recent work in mice has shown that genetic elimination of p16-positive senescent cells ameliorated atherosclerosis (Childs et al., 2016) and osteoarthritis (Jeon et al., 2017).”
From Stress, cell senescence and organismal ageing (2018) · cites this paper as Childs et al., 2016
In mice with Ldlr deficiency fed a high-fat diet, treatment with ABT263 led to inhibited atherogenesis and reduced number and average size of plaques.
“A study in mice aged 10 weeks with Ldlr deficiency, fed a high-fat diet (a reliable model of atherosclerosis in mice), and treated once daily with 100 mg/kg ABT263 for 5 days followed by 14 days off treatment on a repeating cycle for 88 days, showed that elimination of senescent cells led to inhibited atherogenesis and reduced the number and average size of plaques.26”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [26]
Dasatinib, quercetin, and other senolytics were discovered using a mechanism-based approach.
“Dasatinib, quercetin, and other senolytics were discovered using a mechanism-based approach.7,26,105”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [26]
Macrophage senescence instigates features of plaque instability, such as elastic fiber defects and fibrous cap thinning in the brachiocephalic artery and descending aorta.
“Additionally, macrophage senescence instigates features of plaque instability, such as elastic fiber defects and fibrous cap thinning in the brachiocephalic artery and descending aorta [47].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [47]
Senescent cardiovascular cells specifically contribute to chronic cardiovascular diseases, including atherosclerosis, abdominal aortic aneurysm, thoracic aortic aneurysm, artery stiffness and heart failure.
“Senescent cardiovascular cells specifically contributes to chronic CVD, including atherosclerosis [47], abdominal aortic aneurysm (AAA) [48], thoracic aortic aneurysm (TAA) [49], artery stiffness [50] and heart failure [51].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [47]
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BackgroundA versatile drug delivery system targeting senescent cells
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BackgroundSenescent Cells: Emerging Targets for Human Aging and Age-Related Diseases
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- Authors
- Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M.
- Affiliations
- Mayo Clinic (US)
- Buck Institute for Research on Aging (US)
- Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA.
- Venue
- Science
- Published
- 2016-10-28
- Volume
- 354
- Issue
- 6311
- Pages
- 472-477
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC5112585
- OpenAlex
- W2544670169
- Semantic Scholar
- d77de7872775bffbfe9acea2fc8c0316e9ec0b20
- Cited by
- 1,195
- References
- 30
- Citations by year
- 2026: 119 · 2025: 111 · 2024: 129 · 2023: 127 · 2022: 137 · 2021: 151 · 2020: 148 · 2019: 106 · 2018: 107 · 2017: 51 · 2016: 4 · 2015: 1
- FWCI
- 53.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- Paul F. Glenn Foundation
- NIH (R01CA96985, CA168709)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- cellular senescence, foam cells, atherosclerosis, macrophages, plaque vulnerability, elastic fiber degradation, fibrous cap thinning, metalloproteinases, senolytics, subendothelial space, inflammatory cytokines, chemokines
- MeSH terms
- Animals, Foam Cells, Mice, Transgenic, Receptors, LDL, Cytokines, Cellular Senescence, Tunica Intima, Chemokines, Cyclin-Dependent Kinase Inhibitor p16, Atherosclerosis, Mice, Plaque, Atherosclerotic
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