Matrilin-3-Primed Adipose-Derived Mesenchymal Stromal Cell Spheroids Prevent Mesenchymal Stromal-Cell-Derived Chondrocyte Hypertrophy. [PDF]
Adipose-derived mesenchymal stromal cells (Ad-MSCs) are a promising tool for articular cartilage repair and regeneration. However, the terminal hypertrophic differentiation of Ad-MSC-derived cartilage is a critical barrier during hyaline cartilage ...
Muttigi MS +5 more
europepmc +2 more sources
A controlled release bupivacaine-alginate construct: Effect on chondrocyte hypertrophy conversion [PDF]
Objective: Osteoarthritis is a degenerative disease of the joint, affecting over 30 million people in the US1. A key characteristic of OA is chondrocyte hypertrophy, characterized by chondrocyte changes to a more rounded and osteoblastic phenotype ...
Mollie S. Davis +8 more
doaj +2 more sources
Prematurely aging mitochondrial DNA mutator mice display subchondral osteopenia and chondrocyte hypertrophy without further osteoarthritis features. [PDF]
Mitochondrial mutations and dysfunction have been demonstrated in several age-related disorders including osteoarthritis, yet its relative contribution to pathogenesis remains unknown.
Geurts J +7 more
europepmc +2 more sources
Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice by inhibiting Sik3
Therapies are needed for the prevention of chondrocyte hypertrophy and thinning of articular cartilage, features of osteoarthritic joint destruction. Here, the authors show that interfering with Sik3 signalling can increase the size of the chondrocyte ...
Yasuhito Yahara +14 more
doaj +2 more sources
Notch signaling controls chondrocyte hypertrophy via indirect regulation of Sox9 [PDF]
RBPjk-dependent Notch signaling regulates both the onset of chondrocyte hypertrophy and the progression to terminal chondrocyte maturation during endochondral ossification.
Hilton, Matthew J +6 more
core +9 more sources
Neuropeptide Y Promotes mTORC1 to Regulate Chondrocyte Proliferation and Hypertrophy.
Peripheral neuropeptide Y (NPY) has been reported to regulate bone metabolism and homeostasis, however its potential roles in growth plate chondrogenesis remain unclear.
Xiaomin Kang +6 more
semanticscholar +3 more sources
Oral administration of EP4-selective agonist KAG-308 suppresses mouse knee osteoarthritis development through reduction of chondrocyte hypertrophy and TNF secretion. [PDF]
Osteoarthritis (OA) is one of the world’s most common degenerative diseases, but there is no disease-modifying treatment available. Previous studies have shown that prostaglandin E2 (PGE2) and PGE2 receptor 4 (EP4) are involved in OA pathogenesis ...
Murahashi Y +11 more
europepmc +2 more sources
The vacuolar H+ ATPase V0 subunit d2 is associated with chondrocyte hypertrophy and supports chondrocyte differentiation [PDF]
Chondrocyte hypertrophy makes important contributions to bone development and growth. We have investigated a number of novel cartilage genes identified in a recent transcriptomic study to determine whether they are differentially expressed between ...
Babatunde A. Ayodele +3 more
doaj +4 more sources
Smad4 deficiency impairs chondrocyte hypertrophy via the Runx2 transcription factor in mouse skeletal development. [PDF]
Chondrocyte hypertrophy is the terminal step in chondrocyte differentiation and is crucial for endochondral bone formation. How signaling pathways regulate chondrocyte hypertrophic differentiation remains incompletely understood.
Yan J +8 more
europepmc +2 more sources
Tyrosine kinases regulate chondrocyte hypertrophy: promising drug targets for Osteoarthritis. [PDF]
Osteoarthritis (OA) is a major health problem worldwide that affects the joints and causes severe disability. It is characterized by pain and low-grade inflammation. However, the exact pathogenesis remains unknown and the therapeutic options are limited.
M. F. Ferrao Blanco +3 more
semanticscholar +3 more sources

