H
Horacio Gómez-Acevedo
Associate Professor
faculty
Biomedical Informatics, College of Medicine
17 h-index
79 pubs
1,321 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Horacio Gómez-Acevedo is an Associate Professor in Biomedical Informatics at the University of Arkansas for Medical Sciences. His research interests include the genetic and molecular underpinnings of bone metabolism and development, as well as the study of adverse infant outcomes related to maternal health. He has published work investigating the role of specific genes and cellular mechanisms in bone mass regulation, including studies on Mmp13 deletion in mesenchymal cells and the impact of Rab33b missense mouse models on bone resorption. Additionally, Gómez-Acevedo has contributed to research examining the effects of soy formula on reproductive health in male piglets and the risk of adverse infant outcomes associated with maternal mental health and substance use disorders. His work is supported by collaborations with researchers such as Mohammed S. Orloff, David W. Ussery, and Yasir Rahmatallah from the University of Arkansas for Medical Sciences, and Ebrahim Jakoet from the University of Arkansas at Little Rock. Gómez-Acevedo has an h-index of 17, with 78 total publications and 1,303 total citations.
Metrics
- h-index: 17
- Publications: 79
- Citations: 1,321
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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A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior (2025)
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MSR68 Development of a Discrete-Time-Updating Algorithm to Predict Cannabis Use Disorder Among Arkansas Medical Marijuana Cardholders (2025)
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MSR2 Developing a Feature Selection Workflow for Variable-Rich Data: A Case Study Utilizing Claims Data to Build Classifiers for the Prediction of Opioid Use Disorder Among Persons Authorized to Purchase Medical Cannabis (2025)
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MSR34 Development of a Novel Approach to Improve Binary Classification Prediction Tasks When Encountering Time-To-Event Data: Performance Comparison of Three Alternative Approaches To Predict Stimulant Use Disorder Among Persons Authorized To Purchase Medical Marijuana (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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An Activation Likelihood Estimation Meta-Analysis of Voxel-Based Morphometry Studies of Chemotherapy-Related Brain Volume Changes in Breast Cancer (2025)
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Exome Sequencing to Identify Novel Susceptibility Genes for Nonsyndromic Split‐Hand/Ft Malformation: A Report From the National Birth Defects Prevention Study (2025)
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Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers (2025)
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Fairness in Low Birthweight Predictive Models: Implications of Excluding Race/Ethnicity (2025)
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Risk of adverse infant outcomes associated with maternal mental health and substance use disorders (2024)
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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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A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation (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)
Grants & Funding
- Birth Defects Study to Evaluate Pregnancy exposureS (BD-STEPS) Core? Arkansas Center and Stillbirth NIH Co-Investigator
- Birth Defects Study to Evaluate Pregnancy exposureS (BD-STEPS) Core? Arkansas Center and Stillbirth NIH Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Tumor Shape Analysis and its Implications on Prognosis and Treatment TRI Translational Research Institute Principal Investigator
- Tumor Shape Analysis and its Implications on Prognosis and Treatment TRI Translational Research Institute Principal Investigator
- RFA-DD-18-001 Birth Defects Study To Evaluate Pregnancy exposures (BD-STEPS) II Core & Component B Steps -Stillbirth NIH Co-Investigator
Collaboration Network
Top Collaborators
Mohammed S. Orloff
16 shared publications
In database
- Exome Sequencing to Identify Novel Susceptibility Genes for Nonsyndromic Split‐Hand/Ft Malformation: A Report From the National Birth Defects Prevention Study
- Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 16 shared publications
Jing Jin
15 shared publications
In database
- Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S3 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 15 shared publications
Yasir Rahmatallah
15 shared publications
In database
- Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S3 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 15 shared publications
Yong‐Moon Park
15 shared publications
In database
- Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S3 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 15 shared publications
David W. Ussery
15 shared publications
In database
- Abstract 1923: A tract of homozygosity analysis reveals methylation-driven <i>CSMD1</i> expression in non-small cell lung cancers
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S3 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 15 shared publications
Ebrahim Jakoet
14 shared publications
In database
- A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S2 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Data from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S3 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
- Supplementary Fig. S4 from A Tracts of Homozygosity Approach Identifies Methylation-Regulated <i>CSMD1</i> Expression Targets in Non–Small Cell Lung Cancers Related to Smoking Behavior
Showing 5 of 14 shared publications
Stavros C. Manolagas
Central Arkansas Veterans Healthcare System
11 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
- Retraction: Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
Showing 5 of 11 shared publications
Michela Palmieri
Central Arkansas Veterans Healthcare System
10 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
- Retraction: Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- Blocking Oxidized Phospholipids Attenuates the Age-Associated, but Not the Ovariectomy- or Unloading- Induced, Bone Loss in Mice
Showing 5 of 10 shared publications
Teenamol E. Joseph
Central Arkansas Veterans Healthcare System
10 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
- Retraction: Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- Blocking Oxidized Phospholipids Attenuates the Age-Associated, but Not the Ovariectomy- or Unloading- Induced, Bone Loss in Mice
Showing 5 of 10 shared publications
Elena Ambrogini
University of Arkansas for Medical Sciences
10 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
- Retraction: Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- Blocking Oxidized Phospholipids Attenuates the Age-Associated, but Not the Ovariectomy- or Unloading- Induced, Bone Loss in Mice
Showing 5 of 10 shared publications
Ha‐Neui Kim
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
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
- Retraction: Deletion of the scavenger receptor Scarb1 in osteoblast progenitors 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
Aaron Warren
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
Intawat Nookaew
University of Arkansas for Medical Sciences
4 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
Maria Almeida
University of Arkansas for Medical Sciences
4 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
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