Claudia C.S. Chini

High Impact

Researcher

University of Arkansas for Medical Sciences

faculty

29 h-index 80 pubs 4,382 cited

Research Areas

Metabolism and Genetic Disorders Genetics, Aging, and Longevity in Model Organisms Mitochondrial Function and Pathology Neuroinflammation and Neurodegeneration Mechanisms Cardiac Function and Risk Factors Health and Medical Research Impacts Molecular Biology Techniques and Applications

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OverviewAI-generated summary

Claudia C.S. Chini's research focuses on NAD+ metabolism and its implications for aging and various pathological conditions. Her work investigates the role of the CD38 glycohydrolase, often referred to as an "NAD sink," in these processes. Publications detail how CD38 suppression can extend lifespan and healthspan in mice, and improve cardiac function by increasing NAD+ levels. Her group has also explored the association between low NAD+ levels and declines in spermatogenesis in aging mice, as well as the critical role of astrocyte NAD+ glycohydrolase in myelin injury and regeneration.

Further research examines how NAD+-dependent metabolic checkpoints regulate hematopoietic stem cell activation and aging. Chini's scholarship metrics include an h-index of 29 and over 4,300 citations across 80 publications, designating her as a highly cited researcher. She leads a research group and collaborates with other faculty members at the University of Arkansas for Medical Sciences, including Aaron Warren, Ha‐Neui Kim, Ana I. Coelho, and Olivia Reyes‐Castro.

Metrics

h-index: 29
Publications: 80
Citations: 4,382

Selected Publications

Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025) DOI
Chronic Cellular <scp>NAD</scp> Depletion Activates a Viral Infection‐Like Interferon Response Through Mitochondrial <scp>DNA</scp> Leakage (2025) DOI
Methylglyoxal Reshapes Hepatic and Adipose Tissue Metabolism and Increases Viability of Lymphocytes (2025) DOI
An NAD+-dependent metabolic checkpoint regulates hematopoietic stem cell activation and aging (2024) DOI
Heavy-chain antibody targeting of CD38 NAD+ hydrolase ectoenzyme to prevent fibrosis in multiple organs (2023) DOI
Supplementary Figure 2 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
Supplementary Figure 6 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
Supplementary Figure Legend from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
Supplementary Figure 1 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway (2023) DOI
supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway (2023) DOI
Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI
CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023) DOI