2 papers
National Institute of Arthritis and Musculoskeletal and Skin DiseasesUS$4.7mVeterans AffairsEuropean Research Council€150k
Uncovering the dual anabolic and anti-catabolic effects of Pyk2 inhibition on bone mass
National Institute of Arthritis and Musculoskeletal and Skin DiseasesIndiana University IndianapolisUS$445.7k2022–2027
Sexually dimorphic regulation of bone mass by the X-linked histone modifier KDM5C
National Institute of Arthritis and Musculoskeletal and Skin DiseasesVan Andel Research InstituteUS$633.1k2024–2029
Different Roles for Colony Stimulating Factor 1 Isoforms in Anabolic Therapy for Low Bone Mass
National Institute of Arthritis and Musculoskeletal and Skin DiseasesYale UniversityUS$639.5k2023–2028
European Research CouncilHebrew University of Jerusalem€150k2025–2026
Improving bone mass and quality in comorbid diabetes and chronic kidney disease
Control of Bone Mass by Progranulin
Veterans AffairsVeterans Affairs Med Ctr San Francisco2016–2025
Kynurenine: a potential link between age-related decreases in bone mass and kidney function
Mice lacking the enzyme MMP14 in bone-forming cells initially gained bone mass when young, but later developed severe bone loss driven by immune cells.Mice lacking the enzyme MMP14 in bone-forming cells initially gained bone mass when young, but later developed severe bone loss driven by immune cells.
In bone marrow stem cells linked to senile osteoporosis, lamin B1 loss triggered a form of cell death that disrupted mitochondria and impaired bone formation.In bone marrow stem cells linked to senile osteoporosis, lamin B1 loss triggered a form of cell death that disrupted mitochondria and impaired bone formation.
Experiments in mice whose ovaries had been removed linked ceruloplasmin deficiency to higher bone mass at the tissue level.Experiments in mice whose ovaries had been removed linked ceruloplasmin deficiency to higher bone mass at the tissue level.
In a mouse model of osteoporosis, silencing a gene or inhibiting its protein reduced the activity of cells that break down bone.In a mouse model of osteoporosis, silencing a gene or inhibiting its protein reduced the activity of cells that break down bone.
Experiments linked reduced bone formation to impaired sugar breakdown, while genetic changes that enhanced the process improved bone-forming cell function in aged mice.Experiments linked reduced bone formation to impaired sugar breakdown, while genetic changes that enhanced the process improved bone-forming cell function in aged mice.
In a four-week mouse experiment, a bone-building hormone enlarged the spaces housing bone cells, while a drug that slows bone breakdown stabilised their local structure.In a four-week mouse experiment, a bone-building hormone enlarged the spaces housing bone cells, while a drug that slows bone breakdown stabilised their local structure.