Evidence map›Paper›PMID 33031925›Full record

ReviewAgeing research reviews2020

Targeting metabolic pathways for extension of lifespan and healthspan across multiple species.

Andrey A Parkhitko, Elizabeth Filine, Stephanie E Mohr, Alexey Moskalev, Norbert Perrimon

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  3. Methionine restriction and mimetics to ameliorate human aging and disease.Trends in endocrinology and metabolism: TEM · 2026
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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

5 authors at 3 institutions in 2 countries.

Andrey A ParkhitkoDepartment of Genetics, Blavatnik Institute, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 336, Boston, MA, 02115, United States; Aging Institute of UPMC and the University of Pittsburgh, Pittsburgh, PA, United States. Electronic address: aparkhitko@pitt.edu.
Elizabeth FilineDepartment of Genetics, Blavatnik Institute, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 336, Boston, MA, 02115, United States.
Stephanie E MohrDepartment of Genetics, Blavatnik Institute, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 336, Boston, MA, 02115, United States.
Alexey MoskalevInstitute of Biology of the Komi Science Center, Ural Branch of Russian Academy of Sciences, Syktyvkar, Russian Federation; Syktyvkar State University, Syktyvkar, Russian Federation; Engelhard Institute for Molecular Biology, Russian Academy of Sciences, Moscow, Russian Federation.
Norbert PerrimonDepartment of Genetics, Blavatnik Institute, Harvard Medical School, 77 Avenue Louis Pasteur, NRB 336, Boston, MA, 02115, United States; Howard Hughes Medical Institute, Boston, MA, United States. Electronic address: perrimon@receptor.med.harvard.edu.
Harvard University · USEngelhardt Institute of Molecular Biology · RUHoward Hughes Medical Institute · US

Funding

Characterization of the Insulin to Autophagy Pathway in MusclesR01AR057352 · NIAMS · HARVARD MEDICAL SCHOOL · PI NORBERT PERRIMON · 2010 to 2026
$8.2M
Studying methionine flux and its role in aging and neurodegenerationR00AG057792 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PARKHITKO, ANDREY A · 2020 to 2022
$871k
Studying methionine flux and its role in aging and neurodegenerationK99AG057792 · NIA · HARVARD MEDICAL SCHOOL · PI PARKHITKO, ANDREY A · 2018 to 2019
$198k
NIAMS NIH HHS R01 AR057352NIA NIH HHS K99 AG057792NIA NIH HHS R00 AG057792
6 · The paper itself

Abstract

Metabolism plays a significant role in the regulation of aging at different levels, and metabolic reprogramming represents a major driving force in aging. Metabolic reprogramming leads to impaired organismal fitness, an age-dependent increase in susceptibility to diseases, decreased ability to mount a stress response, and increased frailty. The complexity of age-dependent metabolic reprogramming comes from the multitude of levels on which metabolic changes can be connected to aging and regulation of lifespan. This is further complicated by the different metabolic requirements of various tissues, cross-organ communication via metabolite secretion, and direct effects of metabolites on epigenetic state and redox regulation; however, not all of these changes are causative to aging. Studies in yeast, flies, worms, and mice have played a crucial role in identifying mechanistic links between observed changes in various metabolic traits and their effects on lifespan. Here, we review how changes in the organismal and organ-specific metabolome are associated with aging and how targeting of any one of over a hundred different targets in specific metabolic pathways can extend lifespan. An important corollary is that restriction or supplementation of different metabolites can change activity of these metabolic pathways in ways that improve healthspan and extend lifespan in different organisms. Due to the high levels of conservation of metabolism in general, translating findings from model systems to human beings will allow for the development of effective strategies for human health- and lifespan extension.

Indexed as

AgingLongevityAnimalsMetabolic Networks and PathwaysMiceModels, BiologicalMutationAgingC. elegansDrosophilaMetabolismMiceYeast

Identifiers

PMID33031925
PMCPMC9038119
OpenAlexW3091220987

What OpenQuestion holds

Textmetadata
LicenceTDM
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.