Nicholas P. Greene Source Confirmed

Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.

Federal Grant PI High Impact

Associate Professor

University of Arkansas at Fayetteville

faculty

28 h-index 188 pubs 3,786 cited

Research Areas

Muscle Physiology and Disorders Cancer-related molecular mechanisms research Mitochondrial Function and Pathology Diet and metabolism studies Genomics and Phylogenetic Studies Birth, Development, and Health Bioinformatics and Genomic Networks Immune Response and Inflammation

Links

ORCID Lab Website

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OverviewAI-generated summary

Nicholas P. Greene's research focuses on the molecular mechanisms underlying skeletal muscle adaptation, atrophy, and disease, with a particular emphasis on cancer cachexia and aging. His work investigates how cellular processes, including mitochondrial function and transcriptional networks, are disrupted in these conditions.

Greene's investigations have explored the sex-specific differences in muscle response to disuse atrophy and cancer cachexia, identifying distinct catabolic signaling pathways and transcriptional disruptions in female mice. He also studies how exercise can counteract the detrimental effects of cancer cachexia on skeletal muscle. His scholarship metrics include an h-index of 28, 188 total publications, and 3,786 total citations, indicating significant contributions to his field. He has served as PI on a $313,850 NIH grant focused on developing targeted approaches for the prevention of cancer cachexia.

Greene collaborates with several researchers at the University of Arkansas at Fayetteville, including Francielly Morena da Silva, Tyrone A. Washington, Ana Regina Cabrera, and Eleanor R. Schrems, with whom he has co-authored numerous publications.

Metrics

h-index: 28
Publications: 188
Citations: 3,786

Selected Publications

Exercise-induced antioxidant programming in oxidative muscle: a critical IL1β-NBR1-p62 axis (2026) DOI
The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus (2025) DOI
Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer (2025) DOI
Sustained Accumulation of Molecular Clock Suppressors Period 1 and Period 2 Promotes C2C12 Myotube Atrophy Through an Autocrine-Mediated Mechanism With Relevance to Androgen Deprivation-Induced Limb Muscle Mass Loss (2025) DOI
Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice (2025) DOI
Landscape of Clinical Trials in Cancer Cachexia: Assessment of Trends From 1995-2024 (2025) DOI
The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth (2024) DOI
Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex (2024) DOI
Mitochondrial-targeted plastoquinone therapy ameliorates early onset muscle weakness that precedes ovarian cancer cachexia in mice (2024) DOI
Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice (2024) DOI
Muscle weakness and mitochondrial stress occur before severe metastasis in a novel mouse model of ovarian cancer cachexia (2024) DOI
Exploring heterogeneity: a dive into preclinical models of cancer cachexia (2024) DOI
Muscle weakness and mitochondrial stress occur before metastasis in a novel mouse model of ovarian cancer cachexia (2024) DOI
The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth (2024) DOI
The mechanosensitive gene <i>arrestin domain containing 2</i> regulates myotube diameter with direct implications for disuse atrophy with aging (2024) DOI