Cited by 153Genetics, Aging, and Longevity in Model OrganismsMetabolism, Diabetes, and CancerMitochondrial Function and Pathology

Tipping the metabolic scales towards increased longevity in mammals

Riera, Celine E., Dillin, Andrew·2015·Nature Cell Biology

Abstract

A hallmark of ageing is dysfunction in nutrient signalling pathways that regulate glucose homeostasis, negatively affecting whole-body energy metabolism and ultimately increasing the organism's susceptibility to disease. Maintenance of insulin sensitivity depends on functional mitochondrial networks, but is compromised by alterations in mitochondrial energy metabolism during ageing. Here we discuss metabolic paradigms that influence mammalian longevity, and highlight recent advances in identifying fundamental signalling pathways that influence metabolic health and ageing through mitochondrial perturbations.

Integrity signals

Registry

Crossref · 10.1038/ncb3107

Cites

116 of 116 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Riera, C. E., & Dillin, A.
Affiliations
Howard Hughes Medical Institute (US)
Corresponding author
Dillin, Andrew
Venue
Nature Cell Biology
Published
2015-02-27
Volume
17
Issue
3
Pages
196-203
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W2063212818
Cited by
153
References
116
Citations by year
2026: 8 · 2025: 12 · 2024: 9 · 2023: 14 · 2022: 12 · 2021: 15 · 2020: 7 · 2019: 12 · 2018: 17 · 2017: 16 · 2016: 21 · 2015: 10
FWCI
1.88
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
American Diabetes Association
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
aging, longevity, nutrient signaling, glucose homeostasis, insulin sensitivity, mitochondrial bioenergetics, mitochondrial dysfunction, metabolic health, mammals
MeSH terms
Animals, Energy Metabolism, Gene Expression Regulation, Glucose, Homeostasis, Humans, Insulin, Insulin Resistance, Longevity, Metabolic Diseases, Mitochondria, Neoplasms, Signal Transduction, Neurodegenerative Diseases, Mitochondrial Proteins, Unfolded Protein Response

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review