Evidence map›Paper›PMID 36611814›Full record

ReviewCells2022

NAD

Lucie Chanvillard, Alessandra Tammaro, Vincenzo Sorrentino

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Dysregulation of Niacin-Derived NADMedicina (Kaunas, Lithuania) · 2025
    Article
  5. Review
  6. Article
  7. The role of NADnpj metabolic health and disease · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023
    Review
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

3 authors at 3 institutions in 3 countries.

Lucie ChanvillardNestlé Institute of Health Sciences, Nestlé Research, 1015 Lausanne, Switzerland.
Alessandra TammaroDepartment of Pathology, Amsterdam UMC location University of Amsterdam, 1105AZ Amsterdam, The Netherlands.
Vincenzo SorrentinoNestlé Institute of Health Sciences, Nestlé Research, 1015 Lausanne, Switzerland.ORCID 0000-0002-7212-370X
Amsterdam University Medical Centers · NLNational University of Singapore · SGNestlé (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Premature aging causes morphological and functional changes in the kidney, leading to chronic kidney disease (CKD). CKD is a global public health issue with far-reaching consequences, including cardio-vascular complications, increased frailty, shortened lifespan and a heightened risk of kidney failure. Dialysis or transplantation are lifesaving therapies, but they can also be debilitating. Currently, no cure is available for CKD, despite ongoing efforts to identify clinical biomarkers of premature renal aging and molecular pathways of disease progression. Kidney proximal tubular epithelial cells (PTECs) have high energy demand, and disruption of their energy homeostasis has been linked to the progression of kidney disease. Consequently, metabolic reprogramming of PTECs is gaining interest as a therapeutic tool. Preclinical and clinical evidence is emerging that NAD

Indexed as

Aging, PrematureRenal Insufficiency, ChronicHumansKidneyNADRenal DialysisNADage-related diseaseschronic kidney diseaseclinical trialskidneymouse modelsNAD+NAD+ precursorspremature renal agingtubular epithelial cells metabolism

Identifiers

PMID36611814
PMCPMC9818486
OpenAlexW4312043163

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.