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Formerly Arkansas
Last published
2023
Sources
OpenAlex · ORCID
Refreshed
2026-10-07
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Filipa Ponte
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Also affiliated: Universidade do Porto (2009–2017); State University of Vale do Acaraú (2007–2008); Rede de Química e Tecnologia (2011–2016); i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto (2017); Instituto de Ciências Biomédicas Albel Salazar (2011–2013)
Formerly Arkansas Postdoctoral fellow, UAMS through 2021.
9 h-index
25 pubs
457 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Filipa Ponte's research focuses on the molecular mechanisms underlying bone loss, particularly in the context of aging and estrogen deficiency. Her work investigates the role of specific cellular components and signaling pathways in maintaining bone homeostasis. Ponte has studied the contribution of mitochondrial Sirt3 to age-related bone loss and the impact of decreased NAD+ levels on osteoprogenitor cells and bone mass. She has also explored the function of RANK ligand in regulating osteoclast gene expression and the effect of Mmp13 deletion in mesenchymal cells on bone mass and cortical bone loss in mice. Ponte has published 27 papers, with a total of 420 citations and an h-index of 9. She has collaborated with researchers at the University of Arkansas for Medical Sciences, including Maria Almeida, Stavros C. Manolagas, Aaron Warren, and Ha‐Neui Kim.
Metrics
- h-index: 9
- Publications: 25
- Citations: 457
Positions
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Senior Postdoctoral Researcher 2022–2024Institut d'Investigació Biomédica de Bellvitge Hereditary Cancer Group, Laboratory of Colorectal Cancer ORCID
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Senior Postdoc Researcher 2021Institut Hospital del Mar d'Investigacions Mèdiques Tumor Vulnerabilities Group ORCID
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Postdoctoral fellow 2017–2021UAMS Medical Center Endocrinology ORCID
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Post-doc researcher 2016–2017Universidade do Porto Instituto de Patologia e Imunologia Molecular Differentiation and Cancer ORCID
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Post-Doc Researcher 2013–2015Faculty of Pharmacy, University of Porto Departament of Biological Sciences, Laboratory of Toxicology ORCID
Selected Publications
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RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression (2023)
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Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency (2022)
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Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency (2022)
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Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice (2021)
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A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging (2021)
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Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors (2020)
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Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice (2020)
Collaboration Network
Top Collaborators
Maria Almeida
Central Arkansas Veterans Healthcare System
7 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice
- RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
Showing 5 of 7 shared publications
Ha‐Neui Kim
University of Arkansas for Medical Sciences
6 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
Showing 5 of 6 shared publications
Srividhya Iyer
University of Arkansas for Medical Sciences (US)
6 shared publications
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
Showing 5 of 6 shared publications
Stavros C. Manolagas
Central Arkansas Veterans Healthcare System
6 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice
- RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
Showing 5 of 6 shared publications
Aaron Warren
University of Arkansas for Medical Sciences
5 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency
Intawat Nookaew
University of Arkansas for Medical Sciences
4 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency
Erin M. Mannen
University of Arkansas for Medical Sciences (US)
3 shared publications
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency
Horacio Gómez-Acevedo
University of Arkansas for Medical Sciences
3 shared publications
In database
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency
Han Li
University of Arkansas for Medical Sciences (US)
2 shared publications
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Mmp-13 deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice
Li Han
University of Arkansas for Medical Sciences (US)
2 shared publications
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
Han Li
University of Arkansas for Medical Sciences (US)
1 shared publication
- Cxcl12 Deletion in Mesenchymal Cells Increases Bone Turnover and Attenuates the Loss of Cortical Bone Caused by Estrogen Deficiency in Mice
Serra Ucer Ozgurel
University of Arkansas for Medical Sciences
1 shared publication
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
Adriana Lelis Carvalho
Biocant
1 shared publication
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
Nükhet Aykin‐Burns
University of Arkansas for Medical Sciences
1 shared publication
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
Kimberly J. Krager
University of Arkansas for Medical Sciences
1 shared publication
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
Similar Researchers
Based on overlapping research topics
Aaron D. Warren
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
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Ha‐Neui Kim
University of Arkansas for Medical Sciences
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Jacob Kordsmeier
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Ilham Kadhim
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Maria Almeida
University of Arkansas for Medical Sciences
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