Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-08-20
Ha‐Neui Kim
Federal Grant PI
High Impact
Associate Professor
Also affiliated: Seoul National University (2006–2012); University of Arkansas Medical Center (2021); New Generation University College (2006–2007); Korea Institute of Oriental Medicine (2012); Central Arkansas Veterans Healthcare System (2013–2023); Bone Health and Osteoporosis Foundation (2014); Carolina Musculoskeletal Institute (2024); Seoul National University Dental Hospital (2008–2023)
Faculty Researcher
Internal Med, College of Medicine
30 h-index
83 pubs
3,317 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Ha-Neui Kim's research focuses on the cellular and molecular mechanisms underlying bone aging and disease, with an emphasis on mitochondrial function and its role in bone homeostasis. Kim's work investigates how factors such as aging, estrogen deficiency, and ionizing radiation contribute to bone loss by affecting bone cells, including osteoclasts and osteoblasts. Recent publications explore the impact of mitochondrial Sirt3 on age-related bone loss and the role of reactive oxygen species in bone cell physiology. Further studies examine the decline in NAD+ levels with aging and its contribution to the loss of osteoprogenitors and bone mass, as well as the function of Piezo1 in stimulating mitochondrial activity.
Metrics
- h-index: 30
- Publications: 83
- Citations: 3,317
Selected Publications
-
Targeting cellular senescence alleviates bone marrow aging (2026)
-
Abstract LB220: Can dietary calcium prevent myeloma onset (2026)
-
Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
-
The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone (2025)
-
Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
-
Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025)
-
Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
-
Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure (2025)
-
Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
-
Oestradiol and osteoclast differentiation: Effects on p53 and mitochondrial metabolism (2024)
-
Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024)
-
TMI-Based Dose-Escalated Bone Marrow Transplantation Can Help Preserve the Bone Marrow Microenvironment and Reduce Cellular Senescence in Old Mice (2023)
-
A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
-
OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts. (2023)
-
Peptidylarginine deiminase 2 plays a key role in osteogenesis by enhancing RUNX2 stability through citrullination (2023)
Federal Grants 2 $752,246 total
NIH
Co-PI
Mar 2024 - Feb 2029
NIH
Contact PI
Aug 2022 - Jul 2027
Role of Mitochondrial Quality Control in Bone Homeostasis and Disease
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- DNA damage in bone cells UAMS Intramural Grant Programs Principal Investigator
- Role of FoxOs in Skeletal Homeostasis- Resubmission - Continuation-Continuation - Continuation - Continuation NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-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
- Estrogen, Androgen, Aging and Bone Loss in Males VA Merit Co-Investigator
- DEAP Awards - H. Kim - UAMS VCRI - FY26 - Musculoskeletal Disintegration RESH Research Administration Principal Investigator
Collaboration Network
Top Collaborators
Maria Almeida
University of Arkansas for Medical Sciences
17 shared publications
In database
- 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
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
Showing 5 of 17 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
- 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 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
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 11 shared publications
Aaron Warren
University of Arkansas for Medical Sciences
9 shared publications
In database
- 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
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
Showing 5 of 9 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
Stavros C. Manolagas
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
- 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 7 shared publications
Qiang Fu
University of Arkansas for Medical Sciences
6 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
- Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure
Showing 5 of 6 shared publications
Michela Palmieri
Central Arkansas Veterans Healthcare System
6 shared publications
In database
- 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.
- Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass
Showing 5 of 6 shared publications
Elena Ambrogini
University of Arkansas for Medical Sciences
6 shared publications
In database
- 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.
- Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass
Showing 5 of 6 shared publications
Teenamol E. Joseph
Central Arkansas Veterans Healthcare System
5 shared publications
In database
- 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]
- Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass
Adriana Lelis Carvalho
University of Arkansas for Medical Sciences
5 shared publications
In database
- The role of reactive oxygen species in bone cell physiology and pathophysiology
- ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts and a target for the anti-osteoclastogenic effects of estrogens
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Oestradiol and osteoclast differentiation: Effects on p53 and mitochondrial metabolism
- The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone
Filipa Ponte
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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)
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 Richardson
University of Arkansas for Medical Sciences (US)
4 shared publications
- 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
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure
Nükhet Aykin‐Burns
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
- Hematopoietic cytoplasmic adaptor protein Hem1 promotes osteoclast fusion and bone resorption in mice
- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure
Similar Researchers
Based on overlapping research topics
Kenneth H Taylor
University of Arkansas at Fayetteville
Mitochondrial Function and Pathology
Metabolism and Genetic Disorders
Immune Response and Inflammation
Jeff D. Thostenson
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Disease Models, Animal
Jinhu Xiong
University of Arkansas for Medical Sciences
Bone Metabolism and Diseases
Mitochondrial Function and Pathology
Disease Models, Animal
Xuehua Li
University of Arkansas for Medical Sciences
Mitochondrial Function and Pathology
Disease Models, Animal
Bone health and treatments
Y. Lucy Liu
University of Arkansas for Medical Sciences
Mitochondrial Function and Pathology
Disease Models, Animal
Metabolism and Genetic Disorders
Wayne Y Lee
University of Arkansas at Fayetteville
Mitochondrial Function and Pathology
Disease Models, Animal
Metabolism and Genetic Disorders