Match tier
Listed
Presence
Current · Arkansas
Last published
2023
Sources
OpenAlex · ORCID
Refreshed
2026-08-20
Stavros C. Manolagas
Federal Grant PI
High Impact
Distinguished Professor
Also affiliated: Naval Medical Center San Diego (1983); Scripps Health (1989); United States Department of Veterans Affairs (1984–1993); University of California, Los Angeles (1983); University of Arkansas Medical Center (1995–2022); Indianapolis Zoo (1993); University of Manchester (1979); University of California San Diego (1980–1990); Central Arkansas Veterans Healthcare System (2000–2023); Richard L. Roudebush VA Medical Center (1993); Geriatric Research Education and Clinical Center (1997–1999); Salford Royal Hospital (1979); University of California San Diego Medical Center (1981–1990); Regional Medical Center (1983); Bone Health and Osteoporosis Foundation (2002–2014); VA Sepulveda Ambulatory Care Center (1983); Scripps Clinic (1989); John L. McClellan Memorial Veterans Hospital (1997–1999); Larue Carter Hospital (1991–1993); Veterans Medical Research Foundation of San Diego (1981–1990); Indiana University Indianapolis (1993); Indiana University School of Medicine (1994); University of Salford (1979); Indiana University – Purdue University Indianapolis (1989–1994); Indiana University (1992)
Faculty Researcher
Internal Med, College of Medicine
85 h-index
183 pubs
29,218 cited
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Stavros C. Manolagas' research focuses on the mechanisms underlying bone loss, particularly as it relates to aging and estrogen deficiency. His work investigates cellular and molecular pathways involved in bone remodeling and density. Recent publications explore the role of mitochondrial Sirt3 in age-associated bone loss and the impact of neutralizing oxidized phospholipids on bone density in mice. Other studies examine the function of RANK ligand in osteoclast gene expression and the effects of deleting specific genes, such as Mmp13 in mesenchymal cells, on bone mass. Manolagas also studies the relationship between immune factors, like anti phosphocholine IgM antibodies, and bone mineral density in human populations.
He leads a research group at the University of Arkansas for Medical Sciences, where he holds the designation of Distinguished Professor in the Department of Internal Medicine. His collaborative network includes several colleagues from the University of Arkansas for Medical Sciences, with whom he has co-authored numerous publications. Manolagas is recognized as a highly cited researcher, evidenced by his h-index of 85 and over 29,000 citations across his 183 publications.
Metrics
- h-index: 85
- Publications: 183
- Citations: 29,218
Selected Publications
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Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
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Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
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Plasma levels of anti phosphocholine IgM antibodies are negatively correlated with bone mineral density in humans (2025)
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OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts. (2023)
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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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Retraction notice to “Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass” [Bone 170(2023) 116702] (2023)
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RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass (2023)
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Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass (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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Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass (2022)
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Neutralization of oxidized phospholipids attenuates age‐associated bone loss 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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Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency (2021)
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Increased marrow adipogenesis does not contribute to age‐dependent appendicular bone loss in female mice (2020)
Federal Grants 1
VA
Contact PI
Jan 2012 - Mar 2021
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Role of FoxOs in Skeletal Homeostasis- Resubmission - Continuation-Continuation - Continuation - Continuation NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-Investigator
- ESTROGENS AND OSTEOCLASTOGENESIS NIH Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Co-Investigator
- HORMONAL CONTROL OF CYTOKINES IN BONE AND STROMAL CELLS NIH Principal Investigator
- Molecular and Cellular Mechanisms of Osteoporosis NIH Principal Investigator
- OSTEOBLAST COMMITMENT AND DIFFERENTIATION BY ANGELS NIH Co-Principal Investigator
- 1,25 DIHYDROXY VITAMIN D3 AND CELLULAR IMMUNITY NIH Principal Investigator
Collaboration Network
Top Collaborators
Ha‐Neui Kim
University of Arkansas for Medical Sciences
10 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
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- <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
Showing 5 of 10 shared publications
Horacio Gómez-Acevedo
University of Arkansas for Medical Sciences
10 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
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- <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 10 shared publications
Michela Palmieri
Central Arkansas Veterans Healthcare System
9 shared publications
In database
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- Plasma levels of anti phosphocholine IgM antibodies are negatively correlated with bone mineral density in humans
- Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass
Showing 5 of 9 shared publications
Elena Ambrogini
Central Arkansas Veterans Healthcare System
9 shared publications
In database
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- Plasma levels of anti phosphocholine IgM antibodies are negatively correlated with bone mineral density in humans
- Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass
Showing 5 of 9 shared publications
Teenamol E. Joseph
Central Arkansas Veterans Healthcare System
7 shared publications
In database
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass
- Retraction notice to “Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass” [Bone 170(2023) 116702]
Showing 5 of 7 shared publications
Charles A. O’Brien
Central Arkansas Veterans Healthcare System
7 shared publications
In database
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass
- Retraction notice to “Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass” [Bone 170(2023) 116702]
- OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts.
Showing 5 of 7 shared publications
Maria Almeida
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
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
- 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
- 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
5 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
- OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts.
Aaron Warren
University of Arkansas for Medical Sciences
4 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
- <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)
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
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
Wen Ling
1 shared publication
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
Kimberly J. Krager
University of Arkansas for Medical Sciences
1 shared publication
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
Kimberly Richardson
1 shared publication
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
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