Roy Morello Institution-verified
Sourced from institutional research profiles (UAMS TRI or ARA).
Professor
faculty
Research Areas
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: 81
- Citations: 4,020
Selected Publications
-
Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function (2026)
-
Impact of short-term housing temperature alteration on metabolic parameters and adipose tissue in female mice (2025)
-
A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta (2024)
-
A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta (2024)
-
The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (2023)
-
A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation (2023)
-
Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2 (2022)
-
Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta (2022)
-
RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis (2022)
-
Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome (2022)
-
The Osteocyte Transcriptome: Discovering Messages Buried Within Bone (2021)
Federal Grants 1 $380,648 total
Grants & Funding
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
Similar Researchers
Based on overlapping research topics