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With a rise in the need to develop anti-aging drugs, a growing number of in vivo studies evaluating the efficacy of potential drug candidates have used doxorubicin-induced aging mice. However, changes in the biomarkers of senescent cells have not been reported in detail in these animals. To lay a foundation for the use of doxorubicin-induced aging mice, we examined the biomarkers of hepatic and renal senescent cells in these mice. We found that the 5 mg/kg doxorubicin dose is optimal to induce cellular senescence in mice. Subsequently, using this dose, we found that doxorubicin-induced an increase in senescence-associated β-galactosidase (SA-β-gal) positive cells in the kidney and lipofuscin accumulation in the liver. Some markers of senescent cells (p21, p16, and γH2AX) were also significantly upregulated by doxorubicin and then counteracted by metformin treatment. These preliminary findings support the application of doxorubicin-induced aging mice as an animal model to evaluate the efficacy of anti-aging drug candidates.
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http://dx.doi.org/10.1016/j.exger.2022.111800 | DOI Listing |
ACS Nano
September 2025
State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, P. R. China.
Cellular senescence is a critical factor in organismal aging and age-related diseases. Nicotinamide adenine dinucleotide (NAD) has been shown to be closely related to the cellular senescence process and holds potential as a senotherapeutic agent. However, its clinical application has been hindered by challenges such as its inability to be directly absorbed by cells, instability, and lack of targeting specificity.
View Article and Find Full Text PDFRedox Biol
August 2025
Institute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, 350, Taiwan; Department of Life Sciences and Institute of Genome Sciences, National Yang Ming Chiao Tung University, Taipei, 112, Taiwan; Center for Healthy Longevity and Aging Sciences, National Yang Ming Chia
Background: Cardiotoxicity of doxorubicin, a chemotherapy medication, remains the most dangerous side effect. CISD2 plays a critical role during cardiac aging.
Objectives: We use a potent CISD2 activator, hesperetin, to ameliorate doxorubicin-induced cardiotoxicity by upregulating CISD2 in mice.
Int J Mol Sci
July 2025
Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 42415, Republic of Korea.
Senescent cells secrete pro-inflammatory cytokines, collectively referred to as the senescence-associated secretory phenotype (SASP). Certain pro-inflammatory SASP factors are known to inhibit the differentiation of bone-forming osteoblast while promoting the differentiation of bone-resorbing osteoclasts, thereby causing osteoporosis. In this study, we screened cabozantinib, a tyrosine kinase inhibitor used to treat medullary thyroid cancer, for its ability to reduce doxorubicin-induced cellular senescence in both osteoblast and osteoclast progenitors.
View Article and Find Full Text PDFCell Biochem Funct
August 2025
Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Florence, Italy.
Senescent cells accumulate with age in organ and tissue causing the decline of functionality and various pathological conditions including cardiovascular disease. Regular exercise induces continuous exposure to lactate that contribute to adaptive process through mitochondrial biogenesis and improve of metabolic process. Lactate accumulation during exercise also appears to be associated with exercise-induced mitochondrial adaptation.
View Article and Find Full Text PDFCell Death Dis
August 2025
Department of Neurosurgery, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Senescence-associated secretory phenotype (SASP) in cancer refers to the bioactive secretome produced by senescence cells in the tumor microenvironment, which could be triggered by therapeutics or local stress conditions. Here, we provided a SASP Score in glioblastoma (GBM) with generating a SASP gene panel to identify the potential small molecular candidate targeting SASP in GBM. The effectiveness of this scoring method was firstly interrogated with our in-house GBM cohort and public datasets, including transcriptomic data from bulk and single cell GBM samples.
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