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Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes
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  • Published: 23 February 2026

Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes

  • Maria Belen Arteaga1 na1,
  • Karyna Tarasova1 na1,
  • Angkana Kidtiwong1,
  • Sinan Gültekin1,
  • Iris Gerner1,2 na2 &
  • …
  • Florien Jenner  ORCID: orcid.org/0000-0002-6977-19841,2 na2 

Cell Death Discovery , Article number:  (2026) Cite this article

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Subjects

  • Osteoarthritis
  • Senescence

Abstract

Osteoarthritis (OA) is a degenerative joint disease characterized by the accumulation of senescent chondrocytes, which drive inflammation and cartilage degradation. However, in vitro models often fail to recapitulate the complexity of OA-associated senescence. This study compares three senescence induction strategies in chondrocytes—replicative senescence (HP), and stress-induced premature senescence (SIPS) via doxorubicin (DOX) and dexamethasone (DEX)—to establish a physiologically relevant in vitro model for OA research. To this end ovine chondrocytes (n = 3) were subjected to serial passaging (to P40) or exposed to optimized concentrations of DOX (50 nM) or DEX (1 µM). Low passage (P3) cells served as controls. Cellular senescence was assessed via proliferation assays, cell cycle analysis, SA-β-gal activity, telomere length, ROS levels, mitochondrial function, transcriptomic profiling (NGS), and high-resolution mass spectrometry proteomic analysis. All models induced key senescence hallmarks including cell cycle and proliferation arrest, increased SA-β-gal activity, and mitochondrial dysfunction. HP cells showed telomere shortening, ROS accumulation, ATP depletion, and SASP secretion. DOX induced strong DNA damage responses and elevated apoptosis markers, while DEX induced senescence without significant ROS or apoptosis, suggesting distinct SIPS mechanisms. Transcriptomics revealed convergent downregulation of oxidative phosphorylation and selenoamino acid metabolism pathways, implicating mitochondrial dysfunction and redox imbalance as shared features. However, HP induced broad transcriptional suppression, also of inflammatory pathways, while DOX and DEX activated immune and SASP-related pathways. Proteomics confirmed divergent secretory profiles, with DOX/DEX increasing SASP-factors and HP enriching matrix proteins. In summary, although all models recapitulate fundamental aspects of senescence, they diverge in stress responses, immune signaling, and apoptosis profiles. HP most closely mimics aging-associated senescence, whereas DOX and DEX model distinct SIPS relevant to oxidative or pharmacological stress. These findings underscore the importance of model selection in senescence-focused OA research and highlight mitochondrial dysfunction as a central mechanistic hub across senescence pathways.

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Data availability

The datasets generated and analysed during the current study are included in the paper and its supplementary materials. Please use the following link for the deposited RNA-Seq data: https://dataview.ncbi.nlm.nih.gov/object/PRJNA1347060?reviewer=cunkk64deujh7e6iggfprgkje0.

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Acknowledgements

The authors acknowledge the Vetcore facility of the University of Veterinary Medicine Vienna, especially Dr. Ursula Reichart and Dr. Stephan Handschuh for their support with Imunofluorescence assays by Zeiss Observer. The authors acknowledge the use of ChatGPT (OpenAI) for linguistic refinement of the manuscript. All intellectual content, data interpretation, and conclusions remain the sole responsibility of the authors.

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Funded by wings4innovation and the KHAN-I technology transfer fund.

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Author notes

  1. These authors contributed equally: Maria Belen Arteaga, Karyna Tarasova.

  2. These authors jointly supervised this work: Iris Gerner, Florien Jenner.

Authors and Affiliations

  1. Department for Small Animals and Horses, Centre for Equine Health and Research, Equine Surgery Unit, Veterinary Tissue Engineering and Regenerative Medicine Laboratory, University of Veterinary Medicine Vienna, Vienna, Austria

    Maria Belen Arteaga, Karyna Tarasova, Angkana Kidtiwong, Sinan Gültekin, Iris Gerner & Florien Jenner

  2. Austrian Cluster for Tissue Regeneration, Vienna, Austria

    Iris Gerner & Florien Jenner

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Contributions

MBA and KT: study design, data acquisition, analysis and interpretation, manuscript preparation; AK and SG: data acquisition; IG: study design, data analysis and interpretation; FJ: study conception and design, data analysis and interpretation, manuscript preparation. All authors reviewed the manuscript.

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Correspondence to Florien Jenner.

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Arteaga, M.B., Tarasova, K., Kidtiwong, A. et al. Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-02961-y

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  • Received: 01 August 2025

  • Revised: 27 November 2025

  • Accepted: 09 February 2026

  • Published: 23 February 2026

  • DOI: https://doi.org/10.1038/s41420-026-02961-y

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