Evidence map›Paper›PMID 33777963›Full record

ArticleFrontiers in cell and developmental biology2021

Targeting the Mitochondria-Proteostasis Axis to Delay Aging.

Andreas Zimmermann, Corina Madreiter-Sokolowski, Sarah Stryeck, Mahmoud Abdellatif

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  11. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
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  17. NADJournal of lipid and atherosclerosis · 2022
    Review
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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

4 authors.

Andreas ZimmermannInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Corina Madreiter-SokolowskiGottfried Schatz Research Center, Medical University of Graz, Graz, Austria.
Sarah StryeckInstitute of Interactive Systems and Data Science, Graz University of Technology, Graz, Austria.
Mahmoud AbdellatifDepartment of Cardiology, Medical University of Graz, Graz, Austria.

Funding

Austrian Science Fund FWF J 4205
6 · The paper itself

Abstract

Human life expectancy continues to grow globally, and so does the prevalence of age-related chronic diseases, causing a huge medical and economic burden on society. Effective therapeutic options for these disorders are scarce, and even if available, are typically limited to a single comorbidity in a multifaceted dysfunction that inevitably affects all organ systems. Thus, novel therapies that target fundamental processes of aging itself are desperately needed. In this article, we summarize current strategies that successfully delay aging and related diseases by targeting mitochondria and protein homeostasis. In particular, we focus on autophagy, as a fundamental proteostatic process that is intimately linked to mitochondrial quality control. We present genetic and pharmacological interventions that effectively extend health- and life-span by acting on specific mitochondrial and pro-autophagic molecular targets. In the end, we delve into the crosstalk between autophagy and mitochondria, in what we refer to as the mitochondria-proteostasis axis, and explore the prospect of targeting this crosstalk to harness maximal therapeutic potential of anti-aging interventions.

Indexed as

aginganti-aging targetsautophagymitochondriaproteostasis

Identifiers

PMID33777963
PMCPMC7991595

What OpenQuestion holds

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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.