Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-08-20
M
Maria Almeida
Federal Grant PI
High Impact
Professor
Faculty Researcher
54 h-index
152 pubs
11,695 cited
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Maria Almeida's research investigates the mechanisms underlying bone loss associated with aging and estrogen deficiency. Her work has explored the role of mitochondrial function, specifically the sirtuin 3 (Sirt3) enzyme, and the contribution of reactive oxygen species to bone cell physiology and pathophysiology. Almeida has also studied the impact of decreased NAD+ levels on osteoprogenitors and bone mass during aging, and the potential of neutralizing oxidized phospholipids to attenuate age-associated bone loss in mice.
Her federally funded research includes projects examining the mechanisms of decreased bone formation with aging, funded by the NIH/National Institute on Aging, and investigating the antagonism of RANKL signaling by estrogen in osteoclasts, supported by the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases. Almeida also leads a research group focused on refining the identification of mesenchymal cell types associated with murine bone, and studies how RANK ligand influences osteoclast gene expression. Her scholarship metrics include an h-index of 54, with 152 total publications and over 11,000 citations. She frequently collaborates with researchers at the University of Arkansas for Medical Sciences, including Charles A. O’Brien, Elena Ambrogini, Olivia Reyes‐Castro, and Hayley M. Sabol.
Metrics
- h-index: 54
- Publications: 152
- Citations: 11,695
Selected Publications
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Protocol for the enrichment of endosteal and periosteal mesenchymal cells from murine bone for single-cell transcriptome analysis (2026)
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Targeting cellular senescence alleviates bone marrow aging (2026)
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A transcriptomic-driven segmentation and cell simulation framework for high-resolution spatial transcriptomics and cell-cell communication (2026)
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IRE1 signaling in osteoprogenitors augments β-catenin activity and physiologic bone accrual (2026)
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The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (2025)
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Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025)
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The adverse effects of chemotherapy on bone mass are not prevented by senolytics (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
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Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness (2025)
Federal Grants 3 $1,263,659 total
NIH
Contact PI
Mar 2024 - Feb 2029
NIH
Contact PI
Sep 2022 - Aug 2024
NIH
Contact PI
Apr 2021 - Dec 2026
Different consequences of cellular aging in cortical versus cancellous bone- Resubmission
Collaboration Network
Top Collaborators
Ha‐Neui Kim
University of Arkansas for Medical Sciences
18 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- The role of reactive oxygen species in bone cell physiology and pathophysiology
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Longitudinal Functional Study of Murine Aging: A Resource for Future Study Designs
Showing 5 of 18 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
13 shared publications
In database
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
Showing 5 of 13 shared publications
Aaron Warren
University of Arkansas for Medical Sciences
12 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- 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
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
Showing 5 of 12 shared publications
Filipa Ponte
University of Arkansas for Medical Sciences
6 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- 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
- <i>Mmp-13</i> 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
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss 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
- <i>Mmp-13</i> 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
Adriana Lelis Carvalho
University of Arkansas for Medical Sciences
6 shared publications
In database
- The role of reactive oxygen species in bone cell physiology and pathophysiology
- ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts and a target for the anti-osteoclastogenic effects of estrogens
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Oestradiol and osteoclast differentiation: Effects on p53 and mitochondrial metabolism
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
Showing 5 of 6 shared publications
Charles A. O’Brien
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Single-cell Transcriptome Analysis Identifies Senescent Osteocytes as Contributors to Bone Destruction in Breast Cancer Metastasis
- 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
Showing 5 of 6 shared publications
Melda Onal
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- 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
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Showing 5 of 6 shared publications
Jinhu Xiong
University of Arkansas for Medical Sciences
5 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- 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
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Srividhya Iyer
University of Arkansas for Medical Sciences (US)
4 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
- <i>Mmp-13</i> 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
Kimberly J. Krager
Pharmaceutical Biotechnology (Czechia)
4 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
Nükhet Aykin‐Burns
Pharmaceutical Biotechnology (Czechia)
4 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
Horacio Gómez-Acevedo
University of Arkansas for Medical Sciences
4 shared publications
In database
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- <i>Mmp-13</i> 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
Olivia Reyes‐Castro
University of Arkansas for Medical Sciences
4 shared publications
In database
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Single-cell Transcriptome Analysis Identifies Senescent Osteocytes as Contributors to Bone Destruction in Breast Cancer Metastasis
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
- Senolytics deplete senescent osteocytes and improve bone health in metastatic breast cancer
Ana I. Coelho
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
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