Dinesh Bhattarai
Sourced from institutional research profiles (UAMS TRI or ARA).
Post Doctoral Fellow
Also affiliated: Huazhong Agricultural University (2015–2020); University of Utah (2026); University of Arkansas Medical Center (2025)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Dinesh Bhattarai's research focuses on understanding disease mechanisms and host-pathogen interactions, with a particular emphasis on molecular and cellular processes. His work has explored the role of specific molecular entities, such as long non-coding RNAs and microRNAs, in regulating cellular functions and their implications in conditions like ovarian cancer and follicular atresia. Bhattarai has also investigated the mechanisms of pattern recognition receptors in bovine mastitis and the modulation of neutrophil homeostasis in sepsis. His research extends to the effects of environmental factors on animal physiology, examining climatic variations on broiler performance and the role of melatonin in animal reproduction. Bhattarai has contributed to the scientific literature through numerous publications and maintains active collaborations within the University of Arkansas for Medical Sciences. His scholarship metrics include an h-index of 14 and over 893 citations.
Metrics
- h-index: 10
- Publications: 33
- Citations: 701
Positions
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Assistant Professor 2026–presentUniversity of Utah Department of Surgery ORCID
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Post Doctoral Fellow 2022–presentUniversity of Arkansas for Medical Sciences Pharmacology and Toxicology Institutional directory
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Post Doctoral Research Fellow 2019–2022Louisania State Univesity School of Veterinary Medicine, Pathobiological Science ORCID
Selected Publications
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Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats (2026)
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Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation (2026)
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Novel interactions between the C5 ‐ C5aR 1 Axis and IF 1: Implications for kidney mitochondrial physiology and ischemia–reperfusion injury (2026)
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Cold Storage Induced Mortalin-Mediated SDHA Proteostasis to Drive Mitochondrial Dysfunction in Kidney Transplants (Abstract ID: 225742) (2026)
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Influence of Hypothermic Machine Perfusion on Markers of Oxidative Stress and Early Tubular Injury in Rat Donor Kidneys Before Transplantation (2026)
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Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats (2025)
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Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys (2025)
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Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat (2025)
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Cold Storage-Induced Proteasome Dysfunction in Rat Kidney Transplants: A Plausible Role of p38MAPK Signaling (Abstract ID: 161861) (2025)
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Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749) (2025)
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Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants (2024)
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Cold Storage-Mediated Activation of P38MAPK-MK2 Axis Induces Kidney Injury after Transplantation (2024)
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Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation (2024)
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Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function (2024)
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Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model (2023)
Collaboration Network
Top Collaborators
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Novel interactions between the C5 ‐ C5aR 1 Axis and IF 1: Implications for kidney mitochondrial physiology and ischemia–reperfusion injury
Showing 5 of 15 shared publications
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model
- Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749)
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
Showing 5 of 6 shared publications
- Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Influence of Hypothermic Machine Perfusion on Markers of Oxidative Stress and Early Tubular Injury in Rat Donor Kidneys Before Transplantation
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model
- Cold Storage-Mediated p38MAPK Activation: A Potential Contributor of Proteasome Dysfunction and Kidney Damage After Transplantation
- Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749)
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Novel interactions between the C5 ‐ C5aR 1 Axis and IF 1: Implications for kidney mitochondrial physiology and ischemia–reperfusion injury
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- Novel interactions between the C5 ‐ C5aR 1 Axis and IF 1: Implications for kidney mitochondrial physiology and ischemia–reperfusion injury
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats
- Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function
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