Evidence map›Paper›PMID 39868046›Full record

ArticleiScience2025

Nicotinamide mononucleotide restores impaired metabolism, endothelial cell proliferation and angiogenesis in old sedentary male mice.

Kevin Kiesworo, Thomas Agius, Michael R Macarthur, Martine Lambelet, Arnaud Lyon, Jing Zhang, Guillermo Turiel, Zheng Fan, Sènan d'Almeida, Korkut Uygun and 7 more

Abstract read
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. RestorinDrug design, development and therapy · 2026
    Article
  5. Review
  6. Article
  7. 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

17 authors.

Kevin KiesworoDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Thomas AgiusDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Michael R MacarthurLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA.
Martine LambeletDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Arnaud LyonTransplantation Centre and Transplantation Immunopathology Laboratory, Department of Medicine, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Jing ZhangDepartment of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
Guillermo TurielDepartment of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
Zheng FanDepartment of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
Sènan d'AlmeidaFlow Cytometry Core Facility, EPFL, Lausanne, Switzerland.
Korkut UygunCenter for Engineering in Medicine, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Heidi YehCenter for Engineering in Medicine, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Sébastien DégliseDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Katrien de BockDepartment of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
Sarah J MitchellLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA.
Alejandro OcampoDepartment of Biomedical Sciences, Lausanne University (UNIL), Lausanne, Switzerland.
Florent AllagnatDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Alban LongchampDepartment of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is accompanied by a decline in neovascularization potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity. Aged EC harvested from the mouse skeletal muscle displayed a pro-angiogenic gene expression phenotype, along with considerable changes in metabolic genes. Metabolomics analysis and

Indexed as

Cellular physiologyMetabolomics

Identifiers

PMID39868046
PMCPMC11763620

What OpenQuestion holds

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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 OpenQuestion graph.