ArticleAging2018
Azithromycin and Roxithromycin define a new family of "senolytic" drugs that target senescent human fibroblasts.
Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.
- Network meta-analysis of pharmacological treatments for idiopathic pulmonary fibrosis: evaluating effects on lung function.Frontiers in pharmacology · 2026Pooled it
- Pooled it
- Suppression of ATM kinase signaling accelerates cellular senescence.Stem cell reports · 2026Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- The Role of Cellular Senescence in Obstructive Airway Diseases: From Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2026Review
- Systematic profiling reveals distinct senescence signatures and regulators across human brain cell types.Nature communications · 2025Article
- Unraveling the meta-hallmarks between senescent and tumor cells: A new perspective for senolytic drug discovery.Acta pharmaceutica Sinica. B · 2025Review
- SenolyticSynergy: An Attention-Based Network for Discovering Novel Senolytic Combinations via Human Aging Genomics.International journal of molecular sciences · 2025Article
- Association of Medication Use and 8-Year Mortality Risk in Patients With Parkinson Disease: Drug-Wide Trial Emulation.Neurology · 2025Observational
- A novel senotherapeutic strategy with azithromycin for preventing endometriosis progression.Reproductive biology and endocrinology : RB&E · 2025Article
- Regulatory Network Inference of Induced Senescent Midbrain Cell Types Reveals Cell Type-Specific Senescence-Associated Transcriptional Regulators.bioRxiv : the preprint server for biology · 2025Article
- Azithromycin Mitigates Tobacco Smoke-Induced Lung Senescence by Modulating the FOXO3A/CCND1 Signaling Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Discovering geroprotectors through the explainable artificial intelligence-based platform AgeXtend.Nature aging · 2025Article
- Hydrogen Peroxide-Releasing Hydrogel-Mediated Cellular Senescence Model for Aging Research.Biomaterials research · 2025Article
- Natural Product-Derived Senotherapeutics: Extraction and Biological Evaluation Techniques.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- The Quest for Eternal Youth: Hallmarks of Aging and Rejuvenating Therapeutic Strategies.Biomedicines · 2024Review
- Senescence in the bone marrow microenvironment: A driver in development of therapy-related myeloid neoplasms.Journal of bone oncology · 2024Article
- Exploring the Interplay between Cellular Senescence, Immunity, and Fibrosing Interstitial Lung Diseases: Challenges and Opportunities.International journal of molecular sciences · 2024Review
- Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we employed a "senolytic" assay system as a screening tool, with the goal of identifying and repurposing FDA-approved antibiotics, for the targeting of the senescent cell population. Briefly, we used two established human fibroblast cell lines (MRC-5 and/or BJ) as model systems to induce senescence, via chronic treatment with a DNA-damaging agent, namely BrdU (at a concentration of 100 μM for 8 days). Cell viability was then monitored by using the SRB assay, to measure protein content. As a consequence of this streamlined screening strategy, we identified Azithromycin and Roxithromycin as two novel clinically-approved senolytic drugs. However, Erythromycin - the very closely-related parent compound - did not show any senolytic activity, highlighting the dramatic specificity of these interactions. Interestingly, we also show that Azithromycin treatment of human fibroblasts was indeed sufficient to strongly induce both aerobic glycolysis and autophagy. However, the effects of Azithromycin on mitochondrial oxygen consumption rates (OCR) were bi-phasic, showing inhibitory activity at 50 μM and stimulatory activity at 100 μM. These autophagic/metabolic changes induced by Azithromycin could mechanistically explain its senolytic activity. We also independently validated our findings using the xCELLigence real-time assay system, which measures electrical impedance. Using this approach, we see that Azithromycin preferentially targets senescent cells, removing approximately 97% of them with great efficiency. This represents a near 25-fold reduction in senescent cells. Finally, we also discuss our current results in the context of previous clinical findings that specifically document the anti-inflammatory activity of Azithromycin in patients with cystic fibrosis - a genetic lung disorder that results in protein mis-folding mutations that cause protein aggregation.
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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.