Biography and Research Information
OverviewAI-generated summary
Aaron Warren's research investigates the molecular mechanisms underlying bone aging and the effects of estrogen deficiency on skeletal health. His work has explored the role of mitochondrial proteins, such as Sirt3, in bone resorption and the contribution of NAD+ levels to age-related bone loss. Warren has also studied the impact of specific gene deletions, like Mmp13 in mesenchymal cells, on bone mass and cortical bone loss. His publications examine the necessity of the NAD salvage pathway in skeletal development and the influence of hematopoietic proteins on osteoclast function. Further research has investigated mitochondrial oxidative stress and autophagy in osteoblast lineage cells concerning bone mechanoresponsiveness and utilized single-cell RNA sequencing to analyze mesenchymal lineage cells in mouse bone during aging. Warren has a notable publication record with key collaborators at the University of Arkansas for Medical Sciences, including Ha-Neui Kim, Maria Almeida, Ana I. Coelho, and Stavros C. Manolagas.
Metrics
- h-index: 7
- Publications: 17
- Citations: 344
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)
Collaboration Network
Top Collaborators
Maria Almeida
University of Arkansas for Medical Sciences
15 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 15 shared publications
Ha‐Neui Kim
University of Arkansas for Medical Sciences
14 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 14 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
7 shared publications
In database
- 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
- <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 7 shared publications
Ana I. Coelho
University of Arkansas for Medical Sciences
6 shared publications
In database
- 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
Filipa Ponte
University of Arkansas for Medical Sciences
5 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
- <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
Stavros C. Manolagas
Central Arkansas Veterans Healthcare System
5 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Blocking Oxidized Phospholipids Attenuates the Age-Associated, but Not the Ovariectomy- or Unloading- Induced, Bone Loss in Mice
- <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
- 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
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
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- Blocking Oxidized Phospholipids Attenuates the Age-Associated, but Not the Ovariectomy- or Unloading- Induced, Bone Loss in Mice
- <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
Gareeballah Osman Adam
University of Arkansas for Medical Sciences (US)
4 shared publications
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts
Wen Ling
Institute for Musculoskeletal Health
3 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
Kimberly Richardson
Institute for Musculoskeletal Health (AU)
3 shared publications
- 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
Similar Researchers
Based on overlapping research topics
Maria Almeida
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Aging and Longevity in Model Organisms
Ankita Chalke
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Metabolism and Genetic Disorders
Scott Stewart
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Metabolism and Genetic Disorders
Disease Mechanisms Research
Ha‐Neui Kim
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Metabolism and Genetic Disorders
Qiang Fu
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Metabolism and Genetic Disorders
Claudia C.S. Chini
University of Arkansas for Medical Sciences
Aging and Longevity in Model Organisms
Metabolism and Genetic Disorders
Disease Mechanisms Research