ArticleAmerican journal of translational research2017
The mTOR-FAK mechanotransduction signaling axis for focal adhesion maturation and cell proliferation.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 43 citations in OpenAlex.
- Elastomeric 3D-Printed Microenvironments Enable Nanonewton Force Measurements in Healthy and Diseased Human Pluripotent Stem Cell-Derived Neuroepithelial Cells.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Integrin-β1/FAK signaling is involved in electrical stimulation to prevent disuse muscular atrophy induced by tail suspension in mice.BMC musculoskeletal disorders · 2026Article
- Everolimus suppresses glucose transporter 3 membrane trafficking to improve therapeutic efficacy of umbilical cord blood-derived mesenchymal stem cell transplantation in diabetic retinopathy.Cell death & disease · 2026Article
- Mechanical Cues Regulate Cargo Sorting and Export at the Golgi.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracorporeal shockwave therapy rescued mouse critical limb ischemia via upregulating GPR120 against inflammation and promoting angiogenesis for restoring the blood flow in ischemic zone-experimental study.International journal of surgery (London, England) · 2025Article
- Skeletal muscle memory: implications for sports, aging and nutrition.Frontiers in nutrition · 2025Review
- The mechanopathology of the tumor microenvironment: detection techniques, molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
- The application of extracorporeal shock wave therapy on stem cells therapy to treat various diseases.Stem cell research & therapy · 2024Review
- Cervical extracellular matrix hydrogel optimizes tumor heterogeneity of cervical squamous cell carcinoma organoids.Science advances · 2024Article
- Extracellular Matrix Cues Regulate Mechanosensing and Mechanotransduction of Cancer Cells.Cells · 2024Review
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- Loss of function of FIP200 in human pluripotent stem cell-derived neurons leads to axonal pathology and hyperactivity.Translational psychiatry · 2023Article
- Bioinformatics analysis of lncRNA-related ceRNA networks in the peripheral blood lymphocytes of Kazakh patients with essential hypertension in Xinjiang.Frontiers in cardiovascular medicine · 2023Article
- Article
- Human induced mesenchymal stem cells display increased sensitivity to matrix stiffness.Scientific reports · 2022Article
- Mechanomodulation: Physical Treatment Modalities Employ Mechanotransduction to Improve Scarring.European burn journal · 2022Article
- New Frontiers of Extracorporeal Shock Wave Medicine in Urology from Bench to Clinical Studies.Biomedicines · 2022Review
- mTOR Signaling Components in Tumor Mechanobiology.International journal of molecular sciences · 2022Review
- Extracorporeal Shock Wave Therapy Salvages Critical Limb Ischemia in B6 Mice through Upregulating Cell Proliferation Signaling and Angiogenesis.Biomedicines · 2022Article
- Application of extracorporeal shock wave therapy in nervous system diseases: A review.Frontiers in neurology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMechanotransduction (MTD) is an important physiopathological signalling pathway associated with cardiovascular disease such as hypertension. Phosphorylation of focal adhesion kinase (FAK) is a MTD-sensing protein. This study tested the hypothesis that mTOR-FAK MTD signaling axis was crucial for focal adhesion (FA) maturation and cell proliferation.
methodsShock-wave was adopted as a tool for MTD and mTOR-FAK signaling.
resultsAfter demonstrating a failure in FAK phosphorylation after microfilament depolymerization, we attempted to identify the upstream regulator out of three kinases known to be activated in pressure-stimulated MTD [i.e., GSK-3β, Akt, and mTORC1 (mammalian target of rapamycin complex 1)]. Of the three specific inhibitors, only rapamycin, an inhibitor of mTORC1, was found to inhibit FAK phosphorylation, suggesting that mTORC1 is the upstream regulator in shock-wave-elicited FAK phosphorylation. Moreover, mTOR and its readout protein S6K were found to be activated by shock-wave stimulation. On the other hand, microscopic examination revealed not only MTD-induced increase in the number of actin stress fibers, but also alternative subcellular localization of mTORC1 as vesicle-like inclusions on microfilaments. Besides, rapamycin was found to destruct the granular pattern of mTORC1, while dissociation between F-actin and mTORC1 was noted after cytochalasin D administration. Since mTORC1 and FAK are essential for cell proliferation, we performed proliferation assay for mesenchymal stem cell (MSC) with and without shock-wave administration/rapamycin treatment/FAK depletion. The results demonstrated significant enhancement of cell proliferation after shock-wave stimulation but remarkable suppression after rapamycin and siFAK treatment.
conclusionOur findings suggest not only a co-ordinated regulation of FAK phosphorylation by mTORC1 and microfilaments, but also the participation of mTORC1-FAK signalling in MSC proliferation.
Indexed as
Identifiers
28469768PMC5411911W2913318278What OpenQuestion holds
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.