ArticleOsteoarthritis and cartilage2017
Suppression of Sestrins in aging and osteoarthritic cartilage: dysfunction of an important stress defense mechanism.
Article in Osteoarthritis and cartilage, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Meta-analysis Integrated With Multi-omics Data Analysis to Elucidate Pathogenic Mechanisms of Age-Related Knee Osteoarthritis in Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Pooled it
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- Effects and mechanism of sestrin1 protein on osteoarthritis inflammation: A cellular model study.Irish journal of medical science · 2026Article
- MK8722 alleviates osteoarthritis by activating Sesn2 and transcriptionally upregulating BNIP3 to promote mitophagy and inhibit chondrocyte ferroptosis.Journal of advanced research · 2026Article
- Review
- Advances in Regenerative Therapies for Inflammatory Arthritis: Exploring the Potential of Mesenchymal Stem Cells and Extracellular Vesicles.International journal of molecular sciences · 2025Review
- The association between dietary fiber intake and osteoarthritis: a cross-sectional study from the 1999-2018 U.S. National Health and Nutrition Examination Survey.Journal of orthopaedic surgery and research · 2025Article
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
- Mesenchymal stem cell-derived exosomes as a promising cell-free therapy for knee osteoarthritis.Frontiers in bioengineering and biotechnology · 2024Review
- Dietary fiber may benefit chondrocyte activity maintenance.Frontiers in cellular and infection microbiology · 2024Article
- Sestrin2 in diabetes and diabetic complications.Frontiers in endocrinology · 2023Review
- SESN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling.Molecular medicine reports · 2022Article
- The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022Review
- Bone Mesenchymal Stem Cell-Derived Extracellular Vesicles Containing Long Noncoding RNA NEAT1 Relieve Osteoarthritis.Oxidative medicine and cellular longevity · 2022Article
- Association between serum Sestrin2 level and diabetic peripheral neuropathy in type 2 diabetic patients.World journal of clinical cases · 2021Article
- TGFβ1 signaling protects chondrocytes against oxidative stress via FOXO1-autophagy axis.Osteoarthritis and cartilage · 2021Article
- Methylsulfonylmethane enhances MSC chondrogenic commitment and promotes pre-osteoblasts formation.Stem cell research & therapy · 2021Article
- Deer antler extract potentially facilitates xiphoid cartilage growth and regeneration and prevents inflammatory susceptibility by regulating multiple functional genes.Journal of orthopaedic surgery and research · 2021Article
- Whole-Transcriptome Sequence of Degenerative Meniscus Cells Unveiling Diagnostic Markers and Therapeutic Targets for Osteoarthritis.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesAging is an important osteoarthritis (OA) risk factor and compromised stress defense responses may mediate this risk. The Sestrins (Sesn) promote cell survival under stress conditions and regulate AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signaling. This study examined Sesn expression in normal and OA cartilage and functions of Sesn in chondrocytes.
methodsSesn expression in human and mouse normal and OA cartilage was analyzed by quantitative polymerase chain reaction (PCR) and immunohistochemistry. Sesn function was investigated by using small interfering RNA (siRNA) mediated Sesn knockdown and overexpression with analysis of cell survival, gene expression, autophagy, and AMPK and mTOR activation.
resultsSesn mRNA levels were significantly reduced in human OA cartilage and immunohistochemistry of human and mouse OA cartilage also showed a corresponding reduction in protein levels. In cultured human chondrocytes Sesn1, 2 and 3 were expressed and increased by tunicamycin, an endoplasmic reticulum (ER) stress response inducer and 2-deoxyglucose (2DG), a metabolic stress inducer. Sesn1 and 2 were increased by tBHP, an oxidative stress inducer. Sesn knockdown by siRNA reduced chondrocyte viability under basal culture conditions and in the presence of 2DG. Sesn overexpression enhanced LC3-II formation and autophagic flux, and this was related to changes in mTOR but not AMPK activation.
conclusionThese findings are the first to show that Sesn expression is suppressed in OA affected cartilage. Sesn support chondrocyte survival under stress conditions and promote autophagy activation through modulating mTOR activity. Suppression of Sesn in OA cartilage contributes to deficiency in an important cellular homeostasis mechanism.
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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.