Evidence map›Paper›PMID 40418971›Full record

ReviewHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme2025

Asymmetric Dimethylarginine: A Never-Aging Story.

Natalia Jarzebska, Stefan R Bornstein, Sergey Tselmin, Ulrich Julius, Barbara Cellini, Richard Siow, Mike Martin, Rajeshwar P Mookerjee, Arduino A Mangoni, Norbert Weiss and 1 more

Erratum issuedAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Natalia JarzebskaDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Stefan R BornsteinDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Sergey TselminDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Ulrich JuliusDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Barbara CelliniDepartment of Medicine and Surgery, University of Perugia, Perugia, Italy.
Richard SiowSchool of Cardiovascular and Metabolic Medicine and Sciences, Faculty of Life Sciences & Medicine, King's College London, London, United Kingdom of Great Britain and Northern Ireland.
Mike MartinDepartment of Psychology, University of Zurich, Zurich, Switzerland.
Rajeshwar P MookerjeeInstitute of Liver and Digestive Health, University College London, London, United Kingdom of Great Britain and Northern Ireland.
Arduino A MangoniDepartment of Clinical Pharmacology, College of Medicine and Public Health, Flinders University and Flinders Medical Centre, Adelaide, Australia.
Norbert WeissDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.
Roman N RodionovDepartment of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany.ORCID 0000-0002-7470-7776

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human aging is intrinsically associated with the onset and the progression of several disease states causing significant disability and poor quality of life. Although such association was traditionally considered immutable, recent advances have led to a better understanding of several critical biochemical pathways involved in the aging process. This, in turn, has stimulated a significant body of research to investigate whether reprogramming these pathways could delay the progression of human ageing and/or prevent relevant disease states, ultimately favoring healthier aging process. Cellular senescence is regarded as the principal causative factor implicated in biological and pathophysiological processes involved in aging. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase and an independent risk factor for several age-associated diseases. The selective extracorporeal removal of ADMA is emerging as a promising strategy to reduce the burden of age-associated disease states. This article discusses the current knowledge regarding the critical pathways involved in human aging and associated diseases and the possible role of ADMA as a target for therapies leading to healthier aging processes.

Indexed as

AgingArginineAnimalsCellular SenescenceHumansNitric Oxide SynthaseArginineNitric Oxide SynthaseN,N-dimethylarginine

Identifiers

PMID40418971
PMCPMC12638184

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.