Ha‐Neui Kim
Federal Grant PI
High Impact
Associate Professor
faculty
Internal Med, College of Medicine
29 h-index
82 pubs
3,219 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Ha-Neui Kim is an Associate Professor in the Department of Internal Medicine at the University of Arkansas for Medical Sciences. Her research focuses on the molecular mechanisms underlying bone aging and diseases such as osteoporosis. She investigates the roles of mitochondrial function, reactive oxygen species, and specific signaling pathways in bone cell physiology and pathophysiology.
Dr. Kim's work has been supported by federal grants from the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases. One grant, totaling $302,940, supports her investigation into the "Role of Mitochondrial Quality Control in Bone Homeostasis and Disease." She is also a Co-PI on a $409,714 grant examining "Antagonism of RANKL signaling by estrogen in osteoclasts."
Her scholarship metrics include an h-index of 29 and over 3,160 citations across 81 publications. Dr. Kim actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Maria Almeida, Aaron Warren, Charles A. O’Brien, and Stavros C. Manolagas, with whom she has co-authored numerous publications.
Metrics
- h-index: 29
- Publications: 82
- Citations: 3,219
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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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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Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (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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Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
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Oestradiol and osteoclast differentiation: Effects on p53 and mitochondrial metabolism (2024)
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Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024)
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TMI-Based Dose-Escalated Bone Marrow Transplantation Can Help Preserve the Bone Marrow Microenvironment and Reduce Cellular Senescence in Old Mice (2023)
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A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
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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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Peptidylarginine deiminase 2 plays a key role in osteogenesis by enhancing RUNX2 stability through citrullination (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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The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (2023)
Federal Grants 2 $735,416 total
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
Co-PI
Mar 2024 - Feb 2029
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
Contact PI
Aug 2022 - Jul 2027
Role of Mitochondrial Quality Control in Bone Homeostasis and Disease
Grants & Funding
- DNA damage in bone cells UAMS Intramural Grant Programs Principal Investigator
- Antagonism of RANKL signaling by estrogen in osteoclasts NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- Role of Mitochondrial Quality Control in Bone Homeostasis and Disease NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- Role of FoxOs in Skeletal Homeostasis- Resubmission - Continuation-Continuation - Continuation - Continuation NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-Investigator
- Antagonism of RANKL signaling by estrogen in osteoclasts NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- Mechanisms of decreased bone formation with aging NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- Role of Mitochondrial Deacetylase Sirt3 in Skeletal Homeostasis UAMS CMDR Principal Investigator
- Novel role of immunoproteaseome during renal cold storage and transplantation UAMS College of Medicine Principal Investigator
Collaboration Network
Top Collaborators
Maria Almeida
University of Arkansas for Medical Sciences
20 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 20 shared publications
Aaron Warren
University of Arkansas for Medical Sciences
13 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 13 shared publications
Charles A. O’Brien
Central Arkansas Veterans Healthcare System
12 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
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 12 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
11 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Piezo1 stimulates mitochondrial function via <scp>cAMP</scp> signaling
- 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
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Showing 5 of 11 shared publications
Stavros C. Manolagas
University of Arkansas for Medical Sciences
8 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 8 shared publications
Horacio Gómez-Acevedo
University of Arkansas for Medical Sciences
8 shared publications
In database
- 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
- Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass
Showing 5 of 8 shared publications
Jong-Ho Lee
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Kyung-Ok Kim
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Won Jong Jin
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Seungbok Lee
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Hong‐Hee Kim
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Hyunil Ha
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Zang Hee Lee
8 shared publications
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Materials and Methods from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Table 1 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
- Supplementary Figures 1-2 from CXCL10 Promotes Osteolytic Bone Metastasis by Enhancing Cancer Outgrowth and Osteoclastogenesis
Showing 5 of 8 shared publications
Nükhet Aykin‐Burns
University of Arkansas for Medical Sciences
7 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- 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
Showing 5 of 7 shared publications
Kimberly J. Krager
Pharmaceutical Biotechnology (Czechia)
6 shared publications
In database
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Simulated Galactic Cosmic Rays Modify Mitochondrial Metabolism in Osteoclasts, Increase Osteoclastogenesis and Cause Trabecular Bone Loss in Mice
- 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
Showing 5 of 6 shared publications
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