Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-04
C
Claudia C.S. Chini
High Impact
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29 h-index
80 pubs
4,435 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Claudia C.S. Chini's research focuses on the metabolism of nicotinamide adenine dinucleotide (NAD+), a critical coenzyme involved in cellular energy production and signaling pathways. Her work investigates the roles of enzymes such as ADP-ribosyl cyclase 1 (CD38) and NAD+ nucleosidase in various physiological and pathological conditions, including aging, cardiac function, and reproductive health.
Her recent publications explore the implications of NAD+ metabolism in extending lifespan and healthspan in mouse models of aging, as well as its connection to spermatogenesis decline in aging mice. Chini's group has also examined the impact of CD38 suppression on cardiac function and exercise capacity, and the pro-inflammatory effects of dihydronicotinamide riboside, a NAD+ precursor, on macrophages. Furthermore, her research has identified the critical role of astrocyte NAD+ glycohydrolase in myelin injury and regeneration.
Chini leads a research group and has collaborated with researchers at the University of Arkansas for Medical Sciences, including Benjamin M. Stronach, Aaron Warren, Ha-Neui Kim, and Ana I. Coelho. Her scholarship metrics include an h-index of 29, with over 80 publications and 4,435 citations, reflecting her recognition as a highly cited researcher.
Metrics
- h-index: 29
- Publications: 80
- Citations: 4,435
Selected Publications
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Niacin (2026)
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Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025)
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Chronic Cellular <scp>NAD</scp> Depletion Activates a Viral Infection‐Like Interferon Response Through Mitochondrial <scp>DNA</scp> Leakage (2025)
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Methylglyoxal Reshapes Hepatic and Adipose Tissue Metabolism and Increases Viability of Lymphocytes (2025)
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An NAD+-dependent metabolic checkpoint regulates hematopoietic stem cell activation and aging (2024)
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Heavy-chain antibody targeting of CD38 NAD+ hydrolase ectoenzyme to prevent fibrosis in multiple organs (2023)
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Supplementary Figure 2 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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Supplementary Figure 4 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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Supplementary Figure 6 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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Supplementary Figure 3 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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Supplementary Figure Legend from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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Supplementary Figure 1 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
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supplementary figures from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway (2023)
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supplementary figure legends from SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway (2023)
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Supplementary Figure 5 from Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors (2023)
Collaboration Network
Top Collaborators
Eduardo N. Chini
Jacksonville College (US)
71 shared publications
- CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism
- A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline
- The Multi-faceted Ecto-enzyme CD38: Roles in Immunomodulation, Cancer, Aging, and Metabolic Diseases
- Evolving concepts in NAD+ metabolism
- The Pharmacology of CD38/NADase: An Emerging Target in Cancer and Diseases of Aging
Showing 5 of 71 shared publications
Carlos Escande
37 shared publications
- CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism
- Deleted in breast cancer–1 regulates SIRT1 activity and contributes to high-fat diet–induced liver steatosis in mice
- Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Role of Deleted in Breast Cancer 1 (DBC1) Protein in SIRT1 Deacetylase Activation Induced by Protein Kinase A and AMP-activated Protein Kinase
- HDAC3 Is Negatively Regulated by the Nuclear Protein DBC1
Showing 5 of 37 shared publications
Verónica Nin
36 shared publications
- CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism
- Deleted in breast cancer–1 regulates SIRT1 activity and contributes to high-fat diet–induced liver steatosis in mice
- Food Restriction Ameliorates the Development of Polycystic Kidney Disease
- Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Role of Deleted in Breast Cancer 1 (DBC1) Protein in SIRT1 Deacetylase Activation Induced by Protein Kinase A and AMP-activated Protein Kinase
Showing 5 of 36 shared publications
Anatilde M. Gonzalez Guerrico
26 shared publications
- Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- 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
Showing 5 of 26 shared publications
Juliana Camacho-Pereira
21 shared publications
- CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism
- Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Role of Deleted in Breast Cancer 1 (DBC1) Protein in SIRT1 Deacetylase Activation Induced by Protein Kinase A and AMP-activated Protein Kinase
- 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
Showing 5 of 21 shared publications
Maria Thereza Barbosa
20 shared publications
- Targeting of NAD Metabolism in Pancreatic Cancer Cells: Potential Novel Therapy for Pancreatic Tumors
- Deleted in <scp>B</scp>reast <scp>C</scp>ancer 1 regulates cellular senescence during obesity
- 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
Showing 5 of 20 shared publications
Jair Machado Espíndola‐Netto
13 shared publications
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels
- Targeting CD38-dependent NAD+ metabolism to mitigate multiple organ fibrosis
- SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Preclinical efficacy of the novel competitive NAMPT inhibitor STF-118804 in pancreatic cancer
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
Showing 5 of 13 shared publications
Thais Peclat
Jacksonville College (US)
13 shared publications
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels
- The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline
- 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
Showing 5 of 13 shared publications
Gina M. Warner
WinnMed (US)
9 shared publications
- CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism
- A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels
- The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD+ decline
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
Showing 5 of 9 shared publications
Sonu Kashyap
Jacksonville College (US)
9 shared publications
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels
- Evolving concepts in NAD+ metabolism
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- Metalloproteinase PAPP-A regulation of IGF-1 contributes to polycystic kidney disease pathogenesis
- Dihydronicotinamide Riboside Is a Potent NAD+ Precursor Promoting a Pro-Inflammatory Phenotype in Macrophages
Showing 5 of 9 shared publications
Mauro Sola‐Penna
8 shared publications
- SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway
- Preclinical efficacy of the novel competitive NAMPT inhibitor STF-118804 in pancreatic cancer
- 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
Karina S. Kanamori
WinnMed (US)
8 shared publications
- A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions
- Measuring CD38 Hydrolase and Cyclase Activities: 1,N6-Ethenonicotinamide Adenine Dinucleotide (ε-NAD) and Nicotinamide Guanine Dinucleotide (NGD) Fluorescence-based Methods
- Endogenous metabolism in endothelial and immune cells generates most of the tissue vitamin B3 (nicotinamide)
Showing 5 of 8 shared publications
Gourish Mondal
7 shared publications
- 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
- 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
Showing 5 of 7 shared publications
Jin‐San Zhang
7 shared publications
- 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
- 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
Showing 5 of 7 shared publications
Daniel D. Billadeau
7 shared publications
- 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
- 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
Showing 5 of 7 shared publications
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