Humberto Reyes-Pardo
Post Doctoral Fellow
Also affiliated: Autonomous University of San Luis Potosí (2012); Central Arkansas Veterans Healthcare System (2026); Instituto Politécnico Nacional (2019); Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (2019); Tecnológico de Monterrey (2022)
Postdoc Researcher
Internal Med, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Humberto Reyes-Pardo's research focuses on bone metabolism and related cellular processes. He has investigated the role of RANKL-mediated osteoclast formation in bone loss associated with Staphylococcus aureus osteomyelitis, utilizing a murine model. His work also explores the mechanisms contributing to rebound bone resorption following the discontinuation of denosumab, specifically examining the expression of osteoprotegerin by osteocytes.
Reyes-Pardo has also contributed to reviews on the applications of microalgae bioactive compounds and photolyase production, as well as technologies for detecting and treating per- and polyfluoroalkyl substances in wastewater. His research interests extend to the mechanical properties of sensory neurons in the context of diabetes mellitus and its relation to neuropathy. He has published 13 papers, with an h-index of 9 and 372 citations.
Metrics
- h-index: 9
- Publications: 13
- Citations: 386
Selected Publications
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Mechanistic insights into the pathogenesis and therapeutic recalcitrance of <i>Staphylococcus aureus</i> osteomyelitis (2026)
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Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice (2025)
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RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis (2024)
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Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation (2023)
Collaboration Network
Top Collaborators
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
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