Roy Morello
Sourced from institutional research profiles (UAMS TRI or ARA).
Professor
Also affiliated: Baylor University (2006); Baylor College of Medicine (2001–2010); University of Arkansas Medical Center (2018–2021); Harvard University Press (2002); Boys Town National Research Hospital (2002); Tecnologie Avanzate (Italy) (1997–1999); Catholic Biblical Association (1999); Baylor Genetics (2002–2008)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Roy Morello's research focuses on skeletal development and rare genetic disorders, particularly osteogenesis imperfecta (OI) and Smith-McCort dysplasia, utilizing mouse models to investigate underlying molecular mechanisms. His work has explored the genetic basis of these conditions, including the role of collagen mutations and haploinsufficiency in genes like *Col5a1* and *Col1a1*. Morello has also investigated the impact of these mutations on organ systems beyond the skeleton, specifically examining intrinsic lung and respiratory defects associated with type I collagen alterations in OI and Ehlers-Danlos syndrome models.
His laboratory has developed novel mouse models, such as a conditional knock-in model for *Col1a1*, to facilitate the study of OI. Furthermore, his research has delved into the broader cellular processes involved in skeletal health, including the investigation of the NAD salvage pathway in mesenchymal cells and its necessity for skeletal development, as well as the study of osteocyte transcriptomes. Morello's work also extends to the discovery of potential therapeutic targets, such as small molecule agonists for the Relaxin Family Peptide Receptor 2.
Morello is a principal investigator on federal grants, including an NIH/National Heart Lung and Blood Institute award of $380,648 to study lung developmental defects caused by type I collagen mutations in mouse models of osteogenesis imperfecta. He has published extensively, with a h-index of 30 and over 3,972 citations across 81 publications. His collaborations include work with researchers at the University of Arkansas for Medical Sciences, such as Milena Dimori and John L. Carroll.
Metrics
- h-index: 30
- Publications: 83
- Citations: 4,080
Selected Publications
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C107-24 Gata6 and Tcf21: A Yin-Yang Axis Balancing Matrix Integrity and Lipogenic Potential in Alveolar Fibroblasts (2026)
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B74-07 Respiratory Manifestations in Ehlers-Danlos Syndrome and Generalized Hypermobility Spectrum Disorder: Meeting Report and Future Considerations (2026)
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Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function (2026)
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Impact of short-term housing temperature alteration on metabolic parameters and adipose tissue in female mice (2025)
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A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta (2024)
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A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta (2024)
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The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (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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Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2 (2022)
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Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta (2022)
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RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis (2022)
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Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome (2022)
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The Osteocyte Transcriptome: Discovering Messages Buried Within Bone (2021)
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Management of Endocrine Disease: Osteogenesis imperfecta: an update on clinical features and therapies (2020)
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Dental and craniofacial defects in the <i>Crtap<sup>−/−</sup></i> mouse model of osteogenesis imperfecta type VII (2020)
Federal Grants 1 $380,533 total
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Lung alterations in recessive Osteogenesis Imperfecta due to loss of the prolyl 3-hydroxylation complex UAMS 2018 Medical Research Endowment award
- Defining the role of post-translational regulation by extracellular proteases in the pathogenesis of Staphylococcus aureus osteomyelitis NIH
- Elucidating the role of type I collagen mutations on respiratory function in osteogenesis imperfecta. American Lung Association
- Elucidating the role of type I collagen mutations on respiratory function in osteogenesis imperfecta American Lung Association
- Respiratory Function in Animal Models of Skeletal Dysplasias UAMS Research Scholar Pilot Grant Award in Child Health
- Matrix-mediated effects on Bone Marrow Stromal Cells (BMSCs) UAMS 2012 Medical Research Endowment award
- Primary lung defects in mouse models of osteogenesis imperfecta NIH/Nat. Inst. of Child Health & Human Development
- Sc65, a novel osteoporosis related gene ASBMR Junior Faculty Osteoporosis Research Award
- Crtap function during skeletal homeostasis NIH
- Role of the Leprecan Genes in Skeletal Formation NIH
- Morello Startup UAMS College of Medicine
- Targeted Enzyme Replacement Therapy for Rare Forms of Osteogenesis Imperfecta NIH
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences
- Role of collagen prolyl 3-hydroxylation in Osteogenesis imperfecta OSTEOGENESIS IMPERFECTA FOUNDATION - Michael Geisman Research Fellowship
Collaboration Network
Top Collaborators
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
Showing 5 of 6 shared publications
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
- Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2
- RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis
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