SynthesisCell communication and signaling : CCS2023
Meta-analysis of senescent cell secretomes to identify common and specific features of the different senescent phenotypes: a tool for developing new senotherapeutics.
Synthesis in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 28 citations in OpenAlex.
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- A conserved regulatory architecture stabilizes cellular senescence across distinct triggers in human fibroblasts.GeroScience · 2026Article
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- The Interplay Between Cellular Senescence and Lipid Metabolism in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).International journal of molecular sciences · 2026Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- The Impact of Ageing on Fibrillar Collagens.Sub-cellular biochemistry · 2026Review
- Cellular Senescence and SASP in Bladder Ageing: Mechanisms and Emerging Interventions.International journal of general medicine · 2026Review
- Heterogeneity of Cellular Senescence: Subtype-Specific Mechanisms and the Emerging Role of Plasma Membrane Damage.Cancer science · 2025Review
- Replication stress-induced nuclear hypertrophy alters chromatin topology and impacts cancer cell fitness.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges.Cells · 2025Review
- Review
- Is Senolytic Therapy in Cardiovascular Diseases Ready for Translation to Clinics?Biomolecules · 2025Review
- Mechanisms of natural killer cell-mediated clearance of senescent renal tubular epithelial cells.Frontiers in cell and developmental biology · 2025Article
- Mesenchymal Stromal Cell (MSC) Isolation and Induction of Acute and Replicative Senescence.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The senescence-associated secretory phenotype and its physiological and pathological implications.Nature reviews. Molecular cell biology · 2024Review
- SenMayo transcriptomic senescence panel highlights glial cells in the ageing mouse and human retina.npj aging · 2024Article
- IGFBP7 is a key component of the senescence-associated secretory phenotype (SASP) that induces senescence in healthy cells by modulating the insulin, IGF, and activin A pathways.Cell communication and signaling : CCS · 2024Article
- Methods to Investigate the Secretome of Senescent Cells.Methods and protocols · 2024Review
- Senescence-associated secretory phenotype (SASP) and uterine fibroids: Association with PD-L1 activation and collagen deposition.Ageing research reviews · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damage resulting from genotoxic injury can initiate cellular senescence, a state characterized by alterations in cellular metabolism, lysosomal activity, and the secretion of factors collectively known as the senescence-associated secretory phenotype (SASP). Senescence can have beneficial effects on our bodies, such as anti-cancer properties, wound healing, and tissue development, which are attributed to the SASP produced by senescent cells in their intermediate stages. However, senescence can also promote cancer and aging, primarily due to the pro-inflammatory activity of SASP.Studying senescence is complex due to various factors involved. Genotoxic stimuli cause random damage to cellular macromolecules, leading to variations in the senescent phenotype from cell to cell, despite a shared program. Furthermore, senescence is a dynamic process that cannot be analyzed as a static endpoint, adding further complexity.Investigating SASP is particularly intriguing as it reveals how a senescence process triggered in a few cells can spread to many others, resulting in either positive or negative consequences for health. In our study, we conducted a meta-analysis of the protein content of SASP obtained from different research groups, including our own. We categorized the collected omic data based on: i) cell type, ii) harmful agent, and iii) senescence stage (early and late senescence).By employing Gene Ontology and Network analysis on the omic data, we identified common and specific features of different senescent phenotypes. This research has the potential to pave the way for the development of new senotherapeutic drugs aimed at combating the negative consequences associated with the senescence process. Video Abstract.
Indexed as
Identifiers
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.