Meta-hallmarks of aging and cancer

López-Otı́n, Carlos; Pietrocola, Federico; Roiz‐Valle, David; Galluzzi, Lorenzo; Kroemer, Guido

doi:10.1016/j.cmet.2022.11.001

Cited by 168 publications

(135 citation statements)

References 274 publications

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“…Cellular senescence is a process where cells decrease their proliferative capacity and are no longer being able to divide, in association with unique characteristics, such as flattened and enlarged morphology, increased expression of cell cycle inhibitors and elevated senescence-associated β-galactosidase activity [ 22 ]. Notably, the excessive accumulation of senescent cells in different organs and biological systems leads to a functional decline [ 6 , 7 ]. The senescence phenotype is characterized by an aberrant secretome known as the senescence-associated secretory phenotype (SASP).…”

Section: Cellular Senescence In Biological Aging and Age-related Diso...mentioning

confidence: 99%

“…Some non-classical actions of vitamin D may counteract the hallmarks of aging [ 6 , 7 ] ( Figure 1 ). In vitro experiments have shown that 1,25D reduces the harmful effect of progerin on genome stability.…”

Section: Vitamin D Aging and Ckdmentioning

confidence: 99%

“…Loss of proteostasis is another feature of aging [ 7 ]. Vitamin D supplementation promotes protein homeostasis and extends the lifespan of C. elegans by inducing the gene expression of Nrf2-like xenobiotic and oxidative stress-response factor (SKN-1) target genes [ 72 ].…”

Section: Vitamin D Aging and Ckdmentioning

confidence: 99%

“…Aging is a natural and complex process resulting in impaired physiological functions in all cells, tissues and finally organs, resulting in homeostasis loss. The hallmarks of the aging phenotype include genomic instability, telomere shortening, epigenetic changes, loss of proteostasis, dysregulation of the nutrient sensor pathways, mitochondrial dysfunction, stem cell exhaustion, altered intercellular communication, chronic inflammation, dysbiosis and senescence [ 6 , 7 ]. These changes also happen in age-related diseases that share similar pathogenic processes, as described in CKD.…”

Section: Introductionmentioning

confidence: 99%

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Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?

et al. 2023

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As life expectancy increases in many countries, the prevalence of age-related diseases also rises. Among these conditions, chronic kidney disease is predicted to become the second cause of death in some countries before the end of the century. An important problem with kidney diseases is the lack of biomarkers to detect early damage or to predict the progression to renal failure. In addition, current treatments only retard kidney disease progression, and better tools are needed. Preclinical research has shown the involvement of the activation of cellular senescence-related mechanisms in natural aging and kidney injury. Intensive research is searching for novel treatments for kidney diseases as well as for anti-aging therapies. In this sense, many experimental shreds of evidence support that treatment with vitamin D or its analogs can exert pleiotropic protective effects in kidney injury. Moreover, vitamin D deficiency has been described in patients with kidney diseases. Here, we review recent evidence about the relationship between vitamin D and kidney diseases, explaining the underlying mechanisms of the effect of vitamin D actions, with particular attention to the modulation of cellular senescence mechanisms.

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Section: Cellular Senescence In Biological Aging and Age-related Diso...mentioning

confidence: 99%

Section: Vitamin D Aging and Ckdmentioning

confidence: 99%

Section: Vitamin D Aging and Ckdmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?

et al. 2023

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“…Immunotherapy demonstrated high efficacy in clinical trials for tumorigenesis therapy [18], but after long-term treatments, it develops severe immunosuppressive and chemotherapeutic resistance in the tumour microenvironment (TME) [8]. This is due to OS's innate and acquired nature, which causes the therapy's progression to stall [19]. Scientists and clinicians have attempted to solve these problems for the past thirty years [20], but 30% of OS patients still do not respond to these standard treatments [21].…”

Section: Of 26mentioning

confidence: 99%

Relationship between Osteosarcoma Therapy and Tumorigenesis, Metastasis, Immune Evasion, and Chemoresistance

Zaidi¹,

Haque²,

Miskon³

2023

Preprint

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There has been no significant efficacy in treatment for osteosarcoma (OS) metastasis after nearly four decades of trials. This motivates us to elucidate OS therapies according to their four bidirectional mutation stages. To refresh the OS therapy status quo, the historical developments and clinical advancements are briefly described. However, the main issue of metastasis remains unresolved, accounting for 90% of pulmonary metastasis deaths. Thus, this metastasis problem is related to immune evasion and chemoresistance that are being induced after long-term treatment by the use of immunotherapy for tumorigenesis. Therefore, it is rationale to discuss the relationship cycles of mutation stages including tumorigenesis, metastasis, immune evasion, and chemoresistance. Even though many combinational and targeted therapies have been developed to intensify these mutation treatments, successful clinical translations with higher cure rates are still rare. Through this review, an in-depth understanding of the bidirectional relationship between the four OS mutation stages and their respective therapies is provided. Herein, we summarise the medicines used to treat tumorigenesis, including COLGALT2 inhibitors, Tra2B, and AGAP1, miR-148a and miR-21-5p EVs, and the lncRNA LIFR-AS1. Following the medicines used to treat metastasis are AXL, miR-135a-5p, mRNA BCL6, TGFβ1, Tim-3, SOCS5, CASC15, KLF3-AS1, PDCD4, ATG5, and Rab22a-NeoF1. Then the medicines used to treat immune evasion are N-cadherin, anti-IL-9, USP12 inhibitor, IgG-4+ B-cells, LAP inhibitor, anti-Wnt2 mAb, anti-αvβ8 integrin, HK2-mediated IκBα, IDO inhibitor with NO, and TGF-βRII with anti-IgG1. Finally, the medicines used to treat chemoresistance are DHFR, FPGS, HSP-90AA1, XCT-790, ATKI, and IGF1. As a result, this contribution is expected to serve as a reference and guide for scientists and clinicians.

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The Aspirin Conundrum—Navigating Negative Results, Age, Aging Dynamics, and Equity

Mandelblatt,

Mainor,

Hudson

2024

JAMA

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Meta-hallmarks of aging and cancer

Cited by 168 publications

References 274 publications

Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?

Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?

Relationship between Osteosarcoma Therapy and Tumorigenesis, Metastasis, Immune Evasion, and Chemoresistance

The Aspirin Conundrum—Navigating Negative Results, Age, Aging Dynamics, and Equity

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