Ana I. Coelho
Graduate Assistant
Also affiliated: Boston Children's Hospital (2015); Harvard University (2015); University of Lisbon (2013–2015); Universidade do Porto (2023); Maastricht University Medical Centre (2015–2022); Maastricht University (2015–2022); Centro de Investigação em Actividade Física Saúde e Lazer (2023); Manton Center for Orphan Disease Research (2015)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Ana I. Coelho's research focuses on hereditary galactosemia, a group of inherited metabolic disorders affecting galactose metabolism. Her work has involved studying the pathophysiology of classic galactosemia, including an examination of animal and cellular models to identify potential treatment targets. Coelho has also investigated the functional and structural impacts of specific missense mutations associated with classic galactosemia. Her publications address current and future therapeutic strategies for the condition, as well as its natural history, drawing on data from registries. She has also contributed to research on bone metabolism, specifically the role of RANK ligand in osteoclast gene expression.
Metrics
- h-index: 13
- Publications: 20
- Citations: 952
Positions
-
Graduate Assistant 2022–presentUniversity of Arkansas for Medical Sciences Division of Endocrinology and Metabolism ORCID
Selected Publications
-
The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone (2025)
-
Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
-
Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025)
-
The adverse effects of chemotherapy on bone mass are not prevented by senolytics (2025)
-
Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
-
Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness (2025)
-
Differences In Femur And Lumbar Vertebra Adaptations To Running And Swimming In Wistar Rat Models (2024)
-
RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression (2023)
Collaboration Network
Top Collaborators
- RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 7 shared publications
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics
Showing 5 of 6 shared publications
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
Similar Researchers
Based on overlapping research topics