Evidence map›Paper›PMID 32941246›Full record

ReviewCurrent opinion in rheumatology2020

The NADase enzyme CD38: an emerging pharmacological target for systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis.

Thais Ribeiro Peclat, Bo Shi, John Varga, Eduardo Nunes Chini

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Review
  4. Inhibition of CD38 by 78c Enhanced NADInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Article
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  10. Review
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  12. Review
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  14. Article
  15. Review
  16. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  17. Article
  18. NADH/NADBiomolecules · 2021
    Review
  19. Article
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

4 authors at 2 institutions in 1 country.

Thais Ribeiro PeclatSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota.
Bo ShiNorthwestern Scleroderma Program, Feinberg School of Medicine, Northwestern University, Chicago, USA.
John VargaNorthwestern Scleroderma Program, Feinberg School of Medicine, Northwestern University, Chicago, USA.
Eduardo Nunes ChiniSignal Transduction and Molecular Nutrition Laboratory, Kogod Aging Center, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota.
Mayo Clinic · USNorthwestern University · US

Funding

Therapeutic implication of CD38 in CLLR01CA233790 · NCI · MAYO CLINIC JACKSONVILLE · PI CHINI, EDUARDO N · 2019 to 2023
$3.0M
Role of CD38 in NAD metabolism: from the basic biology of aging to translationR01AG058812 · NIA · MAYO CLINIC ROCHESTER · PI CHINI, EDUARDO N · 2018 to 2022
$2.0M
Targeting NAD metabolism to treat systemic sclerosisR21AR074523 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHINI, EDUARDO N, VARGA, JOHN · 2018 to 2019
$396k
NCI NIH HHS R01 CA233790NIAMS NIH HHS R21 AR074523NIA NIH HHS R01 AG058812
6 · The paper itself

Abstract

purpose of reviewHere we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases. We evaluate the potential of targeting CD38 to ameliorate NAD-related metabolic imbalance and tissue dysfunction in the treatment of systemic sclerosis (SSc), systemic lupus erythematous (SLE), and rheumatoid arthritis (RA). RECENT

findingsIn this review, we will discuss emerging basic, preclinical, and human data that point to the novel role of CD38 in dysregulated NAD-homeostasis in SSc, SLE, and RA. In particular, recent studies implicate increased activity of CD38, one of the main enzymes in NAD catabolism, in the pathogenesis of persistent systemic fibrosis in SSc, and increased susceptibility of SLE patients to infections. We will also discuss recent studies that demonstrate that a cytotoxic CD38 antibody can promote clearance of plasma cells involved in the generation of RA antibodies. SUMMARY: Recent studies identify potential therapeutic approaches for boosting NAD to treat rheumatologic diseases including SSc, RA, and SLE, with particular attention to inhibition of CD38 enzymatic activity as a target. Key future directions in the field include the determination of the cell-type specificity and role of CD38 enzymatic activity versus CD38 structural roles in human diseases, as well as the indicators and potential side effects of CD38-targeted treatments.

Indexed as

ADP-ribosyl Cyclase 1Arthritis, RheumatoidHumansLupus Erythematosus, SystemicNAD+ NucleosidaseScleroderma, SystemicADP-ribosyl Cyclase 1NAD+ Nucleosidase

Identifiers

PMID32941246
PMCPMC7807656
OpenAlexW3087311994

What OpenQuestion holds

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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.