ArticleProceedings of the National Academy of Sciences of the United States of America2023
The weakness of senescent dermal fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- From ECM Aging to Mechanobiological Restoration: Injectable Fillers and Dermal Fibroblast Mechanotransduction-A Narrative Review.Gels (Basel, Switzerland) · 2026Review
- Skin aging: mechanisms, evaluation, and rejuvenation.The EMBO journal · 2026Review
- The In Vitro Wound-Scratch Assay: Applications, Technical Advances, and Limitations in Wound Healing Research.International wound journal · 2026Review
- Article
- Dermal Fibroblast Senescence: The Central Hub of Skin Aging-From Intrinsic Dysfunction to Microenvironmental Remodeling.International journal of molecular sciences · 2026Review
- Monopolar Radiofrequency for Dermal Prejuvenation: Scientific Rationale and Mechanisms of Action.Lasers in surgery and medicine · 2026Review
- Tissue turnover and rejuvenation through mechanics.Frontiers in cell and developmental biology · 2026Review
- The cellular senescence-metabolism axis: emerging insights into T cell dynamics in the context of biological aging.Cell communication and signaling : CCS · 2025Review
- Increased substrate stiffness disrupts nuclear-cytoskeletal mechanical coupling in senescent cells.Materials today. Bio · 2025Article
- Metformin promotes wound healing in senescent fibroblasts by regulating SIRT1 and FAP-α.Histochemistry and cell biology · 2025Article
- Endothelial Effects in the Elderly: Fibroblast Regulation in Soft Tissue Healing.Journal of cellular physiology · 2025Article
- The Efficacy and Safety of Combining Cross-Linked Hyaluronic Acid Filler VYC-12L and Energy-Based Devices for Facial Skin Quality Improvement in Asians.Journal of cosmetic dermatology · 2025Article
- Analysis of Beta-Dystroglycan in Different Cell Models of Senescence.International journal of molecular sciences · 2025Article
- Mechanotransduction for therapeutic approaches: Cellular aging and rejuvenation.APL bioengineering · 2025Review
- Human dermal fibroblast senescence in response to single and recurring oxidative stress.Frontiers in aging · 2025Article
- Article
- Applying the Atomic Force Microscopy Technique in Medical Sciences-A Narrative Review.Biomedicines · 2024Review
- 3D Models Currently Proposed to Investigate Human Skin Aging and Explore Preventive and Reparative Approaches: A Descriptive Review.Biomolecules · 2024Review
- Expert Consensus on Big Data Collection of Skin and Appendage Disease Phenotypes in Chinese.Phenomics (Cham, Switzerland) · 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
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skin is the largest human organ with easily noticeable biophysical manifestations of aging. As human tissues age, there is chronological accumulation of biophysical changes due to internal and environmental factors. Skin aging leads to decreased elasticity and the loss of dermal matrix integrity via degradation. The mechanical properties of the dermal matrix are maintained by fibroblasts, which undergo replicative aging and may reach senescence. While the secretory phenotype of senescent fibroblasts is well studied, little is known about changes in the fibroblasts biophysical phenotype. Therefore, we compare biophysical properties of young versus proliferatively aged primary fibroblasts via fluorescence and traction force microscopy, single-cell atomic force spectroscopy, microfluidics, and microrheology of the cytoskeleton. Results show senescent fibroblasts have decreased cytoskeletal tension and myosin II regulatory light chain phosphorylation, in addition to significant loss of traction force. The alteration of cellular forces is harmful to extracellular matrix homeostasis, while decreased cytoskeletal tension can amplify epigenetic changes involved in senescence. Further exploration and detection of these mechanical phenomena provide possibilities for previously unexplored pharmaceutical targets against aging.
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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.