ArticleLife (Basel, Switzerland)2022
Establishment of In Vitro Models by Stress-Induced Premature Senescence for Characterizing the Stromal Vascular Niche in Human Adipose Tissue.
Article in Life (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- A long-term human adipocyte organoid model reveals aging-associated responses to intermittent hypoxia.American journal of physiology. Cell physiology · 2026Article
- Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes.Cell death discovery · 2026Article
- Development of Long-Term Human Adipocyte Organoids Manifesting Aging in Response to Intermittent Hypoxia.bioRxiv : the preprint server for biology · 2025Article
- Generation of a p21 Reporter Mouse and Its Use to Identify and Eliminate p21International journal of molecular sciences · 2023Article
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Authors and funding
11 authors at 4 institutions in 1 country.
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Abstract
Acting as the largest energy reservoir in the body, adipose tissue is involved in longevity and progression of age-related metabolic dysfunction. Here, cellular senescence plays a central role in the generation of a pro-inflammatory environment and in the evolution of chronic diseases. Within the complexity of a tissue, identification and targeting of senescent cells is hampered by their heterogeneity. In this study, we generated stress-induced premature senescence 2D and 3D in vitro models for the stromal vascular niche of human adipose tissue. We established treatment conditions for senescence induction using Doxorubicin (Dox), starting from adipose-derived stromal/stem cells (ASCs), which we adapted to freshly isolated microtissue-stromal vascular fraction (MT-SVF), where cells are embedded within their native extracellular matrix. Senescence hallmarks for the established in vitro models were verified on different cellular levels, including morphology, cell cycle arrest, senescence-associated β-galactosidase activity (SA-βgal) and gene expression. Two subsequent exposures with 200 nM Dox for six days were suitable to induce senescence in our in vitro models. We demonstrated induction of senescence in the 2D in vitro models through SA-βgal activity, at the mRNA level (
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