Match tier
Listed
Presence
Current · Arkansas
Last published
2025
Sources
OpenAlex · ORCID
Refreshed
2026-10-06
R
Robert L. Jilka
High Impact
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Also affiliated: United States Department of Veterans Affairs (1980–1989); University of Kansas (1980); Kansas State University (1975); University of Arkansas Medical Center (1998–2014); Veterans Health Administration (1989); Central Arkansas Veterans Healthcare System (1997–2020); Richard L. Roudebush VA Medical Center (1992–1994); University of Kansas Medical Center (1980–1990); John L. McClellan Memorial Veterans Hospital (1997–1999); Kansas City VA Medical Center (1980–1990); Indiana University Indianapolis (1992–1994); Indiana University School of Medicine (1992–1994); Saint Louis University (1977)
57 h-index
105 pubs
16,846 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Robert L. Jilka's research investigates the relationship between immune system components and bone health. His work includes studies on osteoblasts and osteoclasts, key cell types involved in bone remodeling. One recent publication examines the negative correlation between plasma levels of anti-phosphocholine IgM antibodies and bone mineral density in humans. Jilka has a significant publication record with over 100 articles and a high citation count, reflecting his impact in the field. He has collaborated with several researchers at the University of Arkansas for Medical Sciences, including Elena Ambrogini, Stavros C. Manolagas, Horace J. Spencer, and Lakshmi Menon.
Metrics
- h-index: 57
- Publications: 105
- Citations: 16,846
Selected Publications
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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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Increased marrow adipogenesis does not contribute to age‐dependent appendicular bone loss in female mice (2020)
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A Neutralizing Antibody Targeting Oxidized Phospholipids Promotes Bone Anabolism in Chow-Fed Young Adult Mice (2020)
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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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Elevation of the unfolded protein response increases RANKL expression (2020)
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Cellular actions of parathyroid hormone on bone (2019)
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Oxidation-specific epitopes restrain bone formation (2018)
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Old age causes de novo intracortical bone remodeling and porosity in mice (2017)
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DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age (2017)
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The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct (2016)
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The Road to Reproducibility in Animal Research (2016)
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Skeletal inflammation and attenuation of Wnt signaling, Wnt ligand expression, and bone formation in atherosclerotic ApoE-null mice (2016)
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The Role of Osteocytes in Age-Related Bone Loss (2016)
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The Effects of Androgens on Murine Cortical Bone Do Not Require AR or ERα Signaling in Osteoblasts and Osteoclasts (2015)
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FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation (2014)
Collaboration Network
Top Collaborators
Stavros C. Manolagas
Geriatric Research Education and Clinical Center
45 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Divergent Effects of Selective Peroxisome Proliferator-Activated Receptor-γ2 Ligands on Adipocyte Versus Osteoblast Differentiation
Showing 5 of 45 shared publications
Robert S. Weinstein
Central Arkansas Veterans Healthcare System (US)
39 shared publications
- Matrix-embedded cells control osteoclast formation
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
Showing 5 of 39 shared publications
Charles A. O’Brien
Central Arkansas Veterans Healthcare System
25 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
Showing 5 of 25 shared publications
Maria Almeida
University of Arkansas for Medical Sciences
22 shared publications
In database
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
Showing 5 of 22 shared publications
Teresita Bellido
Central Arkansas Veterans Healthcare System
14 shared publications
In database
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Showing 5 of 14 shared publications
Elena Ambrogini
Central Arkansas Veterans Healthcare System
13 shared publications
In database
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
Showing 5 of 13 shared publications
Stavros C. Manolagas
University of Arkansas for Medical Sciences
13 shared publications
In database
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- The Effects of Androgens on Murine Cortical Bone Do Not Require AR or ERα Signaling in Osteoblasts and Osteoclasts
Showing 5 of 13 shared publications
Paula K. Roberson
Central Arkansas Veterans Healthcare System
12 shared publications
In database
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- FOXOs attenuate bone formation by suppressing Wnt signaling
- Intermittent PTH stimulates periosteal bone formation by actions on post-mitotic preosteoblasts
- Attenuation of the self-renewal of transit-amplifying osteoblast progenitors in the murine bone marrow by 17β-estradiol
Showing 5 of 12 shared publications
A. MICHAEL PARFITT
Central Arkansas Veterans Healthcare System
10 shared publications
In database
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
Showing 5 of 10 shared publications
Ha‐Neui Kim
University of Arkansas for Medical Sciences
9 shared publications
In database
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Old age causes de novo intracortical bone remodeling and porosity in mice
- DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age
- The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
Showing 5 of 9 shared publications
Srividhya V. Iyer
University of Arkansas for Medical Sciences (US)
8 shared publications
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- FOXOs attenuate bone formation by suppressing Wnt signaling
- DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age
- The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
Showing 5 of 8 shared publications
Han Li
University of Arkansas for Medical Sciences (US)
8 shared publications
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
- FOXOs attenuate bone formation by suppressing Wnt signaling
Showing 5 of 8 shared publications
Li Han
University of Arkansas for Medical Sciences (US)
7 shared publications
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age
- Decreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration
- The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
Showing 5 of 7 shared publications
Shoshana M. Bartell
Central Arkansas Veterans Healthcare System (US)
6 shared publications
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- FOXOs attenuate bone formation by suppressing Wnt signaling
- The Effects of Androgens on Murine Cortical Bone Do Not Require AR or ERα Signaling in Osteoblasts and Osteoclasts
- Continuous elevation of PTH increases the number of osteoblasts via both osteoclast-dependent and -independent mechanisms
Showing 5 of 6 shared publications
Scott A. Stewart
Central Arkansas Veterans Healthcare System (US)
6 shared publications
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
- The Skeletal Effects of Glucocorticoid Excess Override Those of Orchidectomy in Mice
- IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice
Showing 5 of 6 shared publications
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