Chu Tao

ORCID: 0009-0003-6069-880X
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About
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Research Areas
  • Cell Adhesion Molecules Research
  • Osteoarthritis Treatment and Mechanisms
  • Cytokine Signaling Pathways and Interactions
  • Erythrocyte Function and Pathophysiology
  • Musculoskeletal pain and rehabilitation
  • Bone Metabolism and Diseases
  • Proteoglycans and glycosaminoglycans research
  • Health Systems, Economic Evaluations, Quality of Life
  • Spine and Intervertebral Disc Pathology
  • Cervical and Thoracic Myelopathy
  • Connective tissue disorders research
  • Fibroblast Growth Factor Research
  • Tendon Structure and Treatment
  • Occupational Health and Performance
  • Inflammatory mediators and NSAID effects
  • Knee injuries and reconstruction techniques
  • Cellular Mechanics and Interactions

Southern University of Science and Technology
2020-2024

Harbin Institute of Technology
2024

Osteoarthritis (OA) is a devastating whole-joint disease affecting large population worldwide with no cure; its mechanism remains poorly defined. Abnormal mechanical stress the main pathological factor of OA. To investigate effects Piezo1 activation on osteoarthritis development and progression to explore Piezo1-targeting OA treatment. The expression levels were determined in human cartilage experimental mice. Mice genetic deletion chondrocytes or intra-articular injection activator Yoda1...

10.1016/j.jare.2023.09.040 article EN cc-by-nc-nd Journal of Advanced Research 2023-09-26

In vertebrates, the type 1 parathyroid hormone receptor (PTH1R) is a critical regulator of skeletal development and homeostasis; however, how it modulated incompletely understood. Here we report that deleting Kindlin-2 in osteoblastic cells using mouse 10-kb Dmp1-Cre largely neutralizes intermittent PTH-stimulated increasing bone volume fraction mineral density by impairing both osteoblast osteoclast formation murine adult bone. Single-cell profiling reveals loss increases proportion...

10.1038/s41392-020-00328-y article EN cc-by Signal Transduction and Targeted Therapy 2020-12-26

The role of osteocytes in maintaining bone mass has been progressively emphasized. Pip5k1c is the most critical isoform among PIP5KIs, which can regulate cytoskeleton, biomembrane, and Ca2+ release cells participate many processes, such as cell adhesion, differentiation, apoptosis. However, its expression function are still unclear. To determine osteocytes, was deleted by breeding 10-kb mouse Dmp1-Cre transgenic mice with Pip5k1cfl/fl mice. Bone histomorphometry, micro-computerized...

10.1016/j.jot.2023.10.008 article EN cc-by-nc-nd Journal of Orthopaedic Translation 2024-03-01

Abstract The progressive destruction of condylar cartilage is a hallmark the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism incompletely understood. Here, we show that Kindlin-2, key focal adhesion protein, strongly detected in cells mandibular mice. We find genetic ablation Kindlin-2 aggrecan-expressing chondrocytes induces multiple spontaneous osteoarthritic lesions, including loss and deformation, surface fissures, ectopic bone formation TMJ. significantly...

10.1038/s41368-022-00185-1 article EN cc-by International Journal of Oral Science 2022-07-04

Abstract Osteocytes act as mechanosensors in bone; however, the underlying mechanism remains poorly understood. Here we report that deleting Kindlin-2 osteocytes causes severe osteopenia and mechanical property defects weight-bearing long bones, but not non-weight-bearing calvariae. loss impairs skeletal responses to stimulation bones. Control cKO mice display similar bone induced by unloading. However, unlike control mice, fail restore lost after reloading. Osteocyte deletion focal adhesion...

10.1038/s42003-021-01950-4 article EN cc-by Communications Biology 2021-03-25

Genetically modified mice are the most useful tools for investigating gene functions in articular cartilage biology and pathogenesis of osteoarthritis. The AggrecanCreERT2 one reported mouse lines used this purpose. Prg4 (proteoglycan 4) encodes lubricin protein is expressed selectively chondrocytes located at superficial layer cartilage. While Prg4GFPCreERT2 knock-in inducible-Cre transgenic were generated a while ago, so far, few studies have line to perform functional biology.We recently...

10.1016/j.jot.2023.05.005 article EN cc-by-nc-nd Journal of Orthopaedic Translation 2023-05-31

Intervertebral disc degeneration (IVDD) is a major cause of low back pain (LBP), worsened by chronic inflammatory processes associated with aging. Tumor necrosis factor alpha (Tnf-α) and its receptors, Tnf receptor type 1 (Tnfr1) 2 (Tnfr2), are upregulated in IVDD. However, pathologic mechanisms remain poorly defined.

10.1002/jsp2.70006 article EN cc-by JOR Spine 2024-10-08

Abstract Objective While joint immobilization is a useful repair method for intra-articular ligament injury and periarticular fracture, prolonged can cause multiple complications. A better understanding how remobilization impact function homeostasis will help clinicians develop novel strategies to reduce Design We first determined the effects of long-term on pain osteophyte formation in patients after an extraarticular fracture or injury. then developed mouse model harvested knee samples at...

10.1186/s13075-023-03223-3 article EN cc-by Arthritis Research & Therapy 2023-12-07

Abstract Osteoarthritis (OA) is an aging-related degenerative joint disease, which has no cure partly due to limited understanding of its pathological mechanism(s). Here we report that the focal adhesion protein Kindlin-2, but not Kindlin-1 or −3, highly expressed in articular chondrocytes hyaline cartilage, dramatically decreased degenerated cartilage aged mice and patients with OA. Inducible deletion Kindlin-2 at adult stage leads spontaneous OA much severe lesions receiving surgery...

10.1101/2021.08.11.456023 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-08-12
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