ArticleGeroScience2023
Increased cellular senescence in doxorubicin-induced murine ovarian injury: effect of senolytics.
Article in GeroScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Ovarian puncture alters genes but not follicle growth in cyclophosphamide mice model.Reproduction & fertility · 2026Article
- Targeting breast cancer senescence in 3D models of bone metastasis.Breast cancer (Tokyo, Japan) · 2026Article
- Senolytics alleviate cyclophosphamide-induced premature ovarian insufficiency by eliminating senescent cells.European journal of histochemistry : EJH · 2026Article
- Necroptosis induced by MLKL overexpression in liver triggers cellular senescence and leads to chronic inflammation and fibrosis.GeroScience · 2026Article
- SIRT5-RAC2 Axis Drives Monocyte-to-Macrophage Differentiation to Promote Inflammatory Injury in Premature Ovarian Insufficiency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Piperine protects ovarian follicles and stromal cells against doxorubicin-induced adverse effects in mouse ovaries.JBRA assisted reproduction · 2026Article
- Decoding the tumor-aging axis: from bench to clinical.Frontiers in immunology · 2026Review
- WWP2-induced inhibition of hepatocellular carcinoma cellular senescence via the ubiquitination and degradation of p21.Cell death & disease · 2025Article
- Mapping the Progression of Therapy-Induced Senescence to Therapy Tolerance: An Evolutionarily Conserved Mechanism for Optimizing Cancer Treatment with Senotherapeutics.ACS pharmacology & translational science · 2025Article
- Flaxseed Lignans Alleviates Doxorubicin-Induced Premature Ovarian Insufficiency in Adult Female Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Modulatory effect of quercetin on premature ovarian insufficiency induced by cyclophosphamide via the PARP1 and GSK3β.Scientific reports · 2025Article
- Protective effect of ammonium trichloride tellurate (AS101) on ovarian injury induced by chemotherapy drug doxorubicin in rats.Journal of ovarian research · 2025Article
- A Comprehensive Multiomics Signature of Doxorubicin-Induced Cellular Senescence in the Postmenopausal Human Ovary.Aging cell · 2025Article
- Functional Features of Senescent Cells and Implications for Therapy.International journal of molecular sciences · 2025Review
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics.Scientific reports · 2025Article
- AMH protects the ovary from doxorubicin by regulating cell fate and the response to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploration of the mechanism and therapy of ovarian aging by targeting cellular senescence.Life medicine · 2025Review
- MiR-668-5p targets ZNRF3, an E3 ubiquitin ligase to enhance osteoblast function and alleviate senescence in doxorubicin-induced age-related bone loss.Frontiers in endocrinology · 2025Article
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
- Loss of p21 does not protect against premature ovarian insufficiency caused by alkylating agents.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian injury caused by chemotherapy can lead to early menopause, infertility, and even premature senility in female cancer patients, impairing the quality of life and overall health of the cancer survivors seriously. However, there is still a lack of effective protection strategies against such injury. Cellular senescence can be induced by chemotherapeutic agents in multiple organs and may corrode the structure and function of normal tissues. We hypothesized that the widely used first-line chemotherapy drug, doxorubicin, could increase senescent cell burden in normal ovarian tissue during the therapeutic process and that elimination of senescent cells with senolytics would ameliorate doxorubicin-induced ovarian injury. Here, we demonstrated an accumulation of cellular senescence in doxorubicin-treated ovaries through detecting p16 and p21 expression levels and senescence-associated β-galactosidase (SA-β-gal) activity as well as senescence-associated secretory phenotype (SASP) factors. Short-term intervention with the classic senolytic combination dasatinib and quercetin (DQ) or fisetin significantly reduced the load of senescent cells in ovaries after doxorubicin treatment. However, neither DQ nor fisetin alleviated doxorubicin-related ovarian dysfunction. Further experiments showed that ovarian apoptosis and fibrosis following doxorubicin exposure could not be improved by senolytics. Collectively, our study shows that senolytic treatment can eliminate accumulated senescent cells, but cannot reverse the massive follicle loss and ovarian stromal fibrosis caused by doxorubicin, suggesting that cellular senescence may not be one of the key mechanisms in doxorubicin-induced ovarian injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.