Match tier
Listed
Presence
Current · Arkansas
Last published
2025
Sources
OpenAlex · ORCID
Refreshed
2026-10-05
Biography and Research Information
OverviewAI-generated summary
Aaron D. Warren's research focuses on the molecular mechanisms underlying bone metabolism and loss, particularly in the context of aging and estrogen deficiency. His work investigates the role of mitochondria, oxidative phosphorylation, and ATP production in osteoclast precursors, and how these processes are influenced by hormonal changes and aging. Warren has published on the contribution of mitochondrial Sirt3 to bone loss and the impact of decreased NAD+ on osteoprogenitors. He also studies the NAD salvage pathway's importance in skeletal development and the mechanisms of mitochondrial reactive oxygen species in bone mesenchymal cells. His collaborators include Ha-Neui Kim, Maria Almeida, Ana I. Coelho, and Stavros C. Manolagas, all at the University of Arkansas for Medical Sciences, with whom he has co-authored multiple publications. Warren holds an h-index of 8 and has published 17 total citations.
Metrics
- h-index: 8
- Publications: 17
- Citations: 388
Positions
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Research Associate III 1997–presentUniversity of Arkansas for Medical Sciences Int. Medicine, Div. of Endocrinoligy ORCID
Selected Publications
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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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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)
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The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (2023)
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Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice (2022)
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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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Hem1 promotes osteoclast fusion and bone resorption in mice (2021)
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<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 (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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Characterization of an alternative oxidase activity of <i>Histoplasma capsulatum</i> (2003)
Collaboration Network
Top Collaborators
Maria Almeida
University of Arkansas for Medical Sciences
13 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
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 13 shared publications
Ha‐Neui Kim
University of Arkansas for Medical Sciences
11 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
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 11 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
8 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
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- 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 8 shared publications
Filipa Ponte
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
- <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
Srividhya Iyer
University of Arkansas for Medical Sciences (US)
5 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
- 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
Md Mohsin Ali
University of Arkansas for Medical Sciences (US)
5 shared publications
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- 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
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics
Ana I. Coelho
University of Arkansas for Medical Sciences
5 shared publications
In database
- 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
- 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 adverse effects of chemotherapy on bone mass are not prevented by senolytics
Stavros C. Manolagas
University of Arkansas Medical Center
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
- <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
Charles A. O’Brien
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
- 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
Adriana Lelis Carvalho
University of Arkansas for Medical Sciences
3 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
Nükhet Aykin‐Burns
University of Arkansas for Medical Sciences
3 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
Kimberly J. Krager
University of Arkansas for Medical Sciences
3 shared publications
In database
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Hem1 promotes osteoclast fusion and bone resorption in mice
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
- <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
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
- <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
Qiang Fu
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Similar Researchers
Based on overlapping research topics
Adriana Lelis Carvalho
University of Arkansas for Medical Sciences
Mitochondrial Function and Pathology
Bone Metabolism and Diseases
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Kimberly J. Krager
University of Arkansas for Medical Sciences
Mitochondrial Function and Pathology
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Nükhet Aykin‐Burns
University of Arkansas for Medical Sciences
Mitochondrial Function and Pathology
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Stavros C. Manolagas
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Disease Mechanisms Research
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Filipa Ponte
University of Arkansas for Medical Sciences
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Bone Metabolism and Diseases
Aging and Longevity in Model Organisms
Charles G Nolan
University of Arkansas at Fayetteville
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