Evidence map›Paper›PMID 29482842›Full record

ReviewTrends in pharmacological sciences2018

The Pharmacology of CD38/NADase: An Emerging Target in Cancer and Diseases of Aging.

Eduardo N Chini, Claudia C S Chini, Jair Machado Espindola Netto, Guilherme C de Oliveira, Wim van Schooten

Abstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 2 pooled it
17.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

138 citing papers in PubMed, 2 syntheses or guidelines pooled it, 228 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. The role of NADnpj metabolic health and disease · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

78 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Eduardo N ChiniSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. Electronic address: chini.eduardo@mayo.edu.
Claudia C S ChiniSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Jair Machado Espindola NettoSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Guilherme C de OliveiraSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Wim van SchootenTeneobio Inc., 1490 O'Brien Drive, Menlo Park, CA 94025, USA.
Mayo Clinic in Arizona · USTenneco (United States) · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D, PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
The Sir2-p53-IGF Link in Mammalian Life-Span ControlR01AG026094 · NIA · UNIVERSITY OF VIRGINIA · PI CHINI, EDUARDO N · 2006 to 2016
$3.8M
Molecular mechanisms of fatty liver disease: role of the protein DBC1R01DK084055 · NIDDK · MAYO CLINIC ROCHESTER · PI CHINI, EDUARDO N · 2009 to 2013
$1.5M
Role of Vav1 protooncogene in pancreatic cancerP20CA102701 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI PETERSEN, GLORIA M. · 2003 to 2003
$1.5M
NCI NIH HHS P20 CA102701NCI NIH HHS P50 CA102701NIA NIH HHS R01 AG026094NIDDK NIH HHS R01 DK084055
6 · The paper itself

Abstract

Recent reports indicate that intracellular NAD levels decline in tissues during chronological aging, and that therapies aimed at increasing cellular NAD levels could have beneficial effects in many age-related diseases. The protein CD38 (cluster of differentiation 38) is a multifunctional enzyme that degrades NAD and modulates cellular NAD homeostasis. At the physiological level, CD38 has been implicated in the regulation of metabolism and in the pathogenesis of multiple conditions including aging, obesity, diabetes, heart disease, asthma, and inflammation. Interestingly, many of these functions are mediated by CD38 enzymatic activity. In addition, CD38 has also been identified as a cell-surface marker in hematologic cancers such as multiple myeloma, and a cytotoxic anti-CD38 antibody has been approved by the FDA for use in this disease. Although this is a remarkable development, killing CD38-positive tumor cells with cytotoxic anti-CD38 antibodies is only one of the potential pharmacological uses of targeting CD38. The present review discusses the biology of the CD38 enzyme and the current state of development of pharmacological tools aimed at CD38, and explores how these agents may represent a novel approach for treating human conditions including cancer, metabolic disease, and diseases of aging.

Indexed as

ADP-ribosyl Cyclase 1AgingAnimalsAntibodiesHumansMolecular Targeted TherapyNADNAD+ NucleosidaseNeoplasmsSmall Molecule LibrariesADP-ribosyl Cyclase 1AntibodiesNADNAD+ NucleosidaseSmall Molecule Librariesagingantibodiescancer and metabolismCD38NAD(+)NADasesirtuinssmall molecules

Identifiers

PMID29482842
PMCPMC5885288
OpenAlexW2788868093

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.