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OverviewAI-generated summary
Claudia C.S. Chini's research focuses on the role of NAD+ metabolism and its associated enzymes, particularly CD38, in aging and various pathological conditions. Her work investigates how disruptions in NAD+ levels impact cellular function, stem cell activation, and organ system health. Recent publications explore the implications of CD38 glycohydrolase activity, examining its function as an "NAD+ sink" and its relevance in disease states.
Chini's group has published studies on the effects of CD38 suppression, demonstrating increased lifespan and healthspan in mouse models of aging, as well as improvements in cardiac function and NAD+ levels. Her research also addresses the decline of spermatogenesis associated with low NAD+ levels in aging mice and investigates the pro-inflammatory effects of specific NAD+ precursors on macrophages. Furthermore, her work has identified a critical role for astrocytic NAD+ glycohydrolase in myelin repair and regeneration following injury.
With an h-index of 29 and over 4,435 citations across 80 publications, Chini is recognized as a highly cited researcher. She leads a research group at the University of Arkansas for Medical Sciences and collaborates with colleagues within the institution, including Aaron Warren, Ha‐Neui Kim, Ana I. Coelho, and Olivia Reyes‐Castro.
Metrics
- h-index: 29
- Publications: 80
- Citations: 4,435
Selected Publications
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Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025)
Collaboration Network
Top Collaborators
Eduardo N. Chini
Mayo Clinic in Florida (US)
40 shared publications
- Evolving concepts in NAD+ metabolism
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- CD38 inhibitor 78c increases mice lifespan and healthspan in a model of chronological aging
- An NAD+-dependent metabolic checkpoint regulates hematopoietic stem cell activation and aging
- Critical Role of Astrocyte NAD <sup>+</sup> Glycohydrolase in Myelin Injury and Regeneration
Showing 5 of 40 shared publications
Carlos Escande
25 shared publications
- Benefits in cardiac function by CD38 suppression: Improvement in NAD+ levels, exercise capacity, heart rate variability and protection against catecholamine-induced ventricular arrhythmias
- Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
Showing 5 of 25 shared publications
Anatilde M. Gonzalez Guerrico
24 shared publications
- Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 24 shared publications
Verónica Nin
24 shared publications
- Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 24 shared publications
Juliana Camacho-Pereira
18 shared publications
- Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Data from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
Showing 5 of 18 shared publications
Maria Thereza Barbosa
18 shared publications
- Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- CCR Translation for This Article from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Data from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
Showing 5 of 18 shared publications
Thais Peclat
Jacksonville College (US)
9 shared publications
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- CD38 inhibitor 78c increases mice lifespan and healthspan in a model of chronological aging
- Critical Role of Astrocyte NAD <sup>+</sup> Glycohydrolase in Myelin Injury and Regeneration
- Benefits in cardiac function by CD38 suppression: Improvement in NAD+ levels, exercise capacity, heart rate variability and protection against catecholamine-induced ventricular arrhythmias
- Dihydronicotinamide Riboside Is a Potent NAD+ Precursor Promoting a Pro-Inflammatory Phenotype in Macrophages
Showing 5 of 9 shared publications
Jair Machado Espíndola‐Netto
8 shared publications
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
- Endogenous Metabolism in Endothelial and Immune Cells Is the Main Source of Tissue Levels of the Vitamin B <sub>3</sub> Nicotinamide
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 8 shared publications
Julianna D. Zeidler
Mayo Clinic in Arizona (US)
6 shared publications
- Evolving concepts in NAD+ metabolism
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- Dihydronicotinamide Riboside Is a Potent NAD+ Precursor Promoting a Pro-Inflammatory Phenotype in Macrophages
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
- Endogenous Metabolism in Endothelial and Immune Cells Is the Main Source of Tissue Levels of the Vitamin B <sub>3</sub> Nicotinamide
Showing 5 of 6 shared publications
Sonu Kashyap
Glenn Foundation for Medical Research (US)
6 shared publications
- Evolving concepts in NAD+ metabolism
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- Dihydronicotinamide Riboside Is a Potent NAD+ Precursor Promoting a Pro-Inflammatory Phenotype in Macrophages
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
- Chronic Cellular <scp>NAD</scp> Depletion Activates a Viral Infection‐Like Interferon Response Through Mitochondrial <scp>DNA</scp> Leakage
Showing 5 of 6 shared publications
Gourish Mondal
6 shared publications
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 6 shared publications
Mauro Sola‐Penna
6 shared publications
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 6 shared publications
Jin‐San Zhang
6 shared publications
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 6 shared publications
Daniel D. Billadeau
6 shared publications
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Data from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
Showing 5 of 6 shared publications
Karina S. Kanamori
WinnMed (US)
4 shared publications
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
- Endogenous Metabolism in Endothelial and Immune Cells Is the Main Source of Tissue Levels of the Vitamin B <sub>3</sub> Nicotinamide
- THE ROLE OF CD38 AS A THERAPEUTIC TARGET FOR PROTECTION AGAINST DOXORUBICIN-INDUCED CARDIOTOXICITY
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