ArticleJCI insight2024
Senotherapeutic drug treatment ameliorates chemotherapy-induced cachexia.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Chemotherapy neurotoxicity and aging: Uncovering shared central nervous system pathologies and potential interventions.Neuro-oncology advances · 2026Review
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Cellular Senescence in Skeletal Muscle Aging.Endocrinology and metabolism (Seoul, Korea) · 2026Review
- Does Time Tick Faster in Cerebral Palsy? Accelerated Aging as a Framework for Skeletal Muscle Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Biomarkers of Cellular Senescence and their Association with Frailty, Clinical Outcomes, and Survival in Multiple Myeloma.Research square · 2026Article
- Senescent Mesenchymal Stromal Cells Differentially Alter Adipogenesis in Adipose Tissue, Skeletal Muscle, and Bone Marrow.Obesity (Silver Spring, Md.) · 2026Article
- NF-κB Signaling as a Central Driver of Cancer Cachexia.Cancers · 2026Review
- Concurrent PIK3CA mutant promotes cachexia through inflammatory signaling in EGFR mutant lung cancer.Nature communications · 2025Article
- Reversing coma by senolytics and stem cells: the future is now.Journal of translational medicine · 2025Review
- The role of adipose tissue in critical illness-induced skeletal muscle wasting-new considerations for treatment approaches.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics.Scientific reports · 2025Article
- Lysosomal Stress in Cardiovascular Diseases: Therapeutic Potential of Cardiovascular Drugs and Future Directions.Biomedicines · 2025Review
- Identification of a senescence-associated transcriptional program in skeletal muscle of cachectic pancreatic-tumor-bearing mice.American journal of physiology. Cell physiology · 2025Article
- Copper-based metal-organic frameworks for antitumor application.Journal of nanobiotechnology · 2025Review
- Nutritional aspects in neuroendocrine neoplasms. bridging the gap between dietary interventions and cancer care strategies: a scoping review.Journal of endocrinological investigation · 2025Article
- Pan-cancer secreted proteome and skeletal muscle regulation: insight from a proteogenomic data-driven knowledge base.Functional & integrative genomics · 2025Review
- Diversity in chemotherapy-induced cachexia.American journal of physiology. Cell physiology · 2025Review
- Emerging insights in senescence: pathways from preclinical models to therapeutic innovations.npj aging · 2024Review
- Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Cachexia is a debilitating skeletal muscle wasting condition for which we currently lack effective treatments. In the context of cancer, certain chemotherapeutics cause DNA damage and cellular senescence. Senescent cells exhibit chronic activation of the transcription factor NF-κB, a known mediator of the proinflammatory senescence-associated secretory phenotype (SASP) and skeletal muscle atrophy. Thus, targeting NF-κB represents a logical therapeutic strategy to alleviate unintended consequences of genotoxic drugs. Herein, we show that treatment with the IKK/NF-κB inhibitor SR12343 during a course of chemotherapy reduces markers of cellular senescence and the SASP in liver, skeletal muscle, and circulation and, correspondingly, attenuates features of skeletal muscle pathology. Lastly, we demonstrate that SR12343 mitigates chemotherapy-induced reductions in body weight, lean mass, fat mass, and muscle strength. These findings support senescent cells as a promising druggable target to counteract the SASP and skeletal muscle wasting in the context of chemotherapy.
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What OpenQuestion holds
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.