Evidence map›Paper›PMID 34926470›Full record

ReviewFrontiers in cell and developmental biology2021

The Interactome in the Evolution From Frailty to Sarcopenic Dependence.

Ana Coto-Montes, Laura González-Blanco, Eduardo Antuña, Iván Menéndez-Valle, Juan Carlos Bermejo-Millo, Beatriz Caballero, Ignacio Vega-Naredo, Yaiza Potes

Open access · goldAbstract readReview
In one paragraph

Review 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 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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

8 authors at 3 institutions in 1 country.

Ana Coto-MontesDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Laura González-BlancoÁrea de Sistemas de Producción Animal, Servicio Regional de Investigación y Desarrollo Agroalimentario (SERIDA), Villaviciosa, Spain.
Eduardo AntuñaDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Iván Menéndez-ValleDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Juan Carlos Bermejo-MilloDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Beatriz CaballeroDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Ignacio Vega-NaredoDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Yaiza PotesDepartment of Cell Biology and Morphology, Faculty of Medicine, University of Oviedo, Oviedo, Spain.
Instituto de Investigación Sanitaria del Principado de Asturias · ESUniversidad de Oviedo · ESServicio Regional de Investigación y Desarrollo Agroalimentario · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biomarkers are essential tools for accurate diagnosis and effective prevention, but their validation is a pending challenge that limits their usefulness, even more so with constructs as complex as frailty. Sarcopenia shares multiple mechanisms with frailty which makes it a strong candidate to provide robust frailty biomarkers. Based on this premise, we studied the temporal evolution of cellular interactome in frailty, from independent patients to dependent ones. Overweight is a recognized cause of frailty in aging, so we studied the altered mechanisms in overweight independent elderly and evaluated their aggravation in dependent elderly. This evidence of the evolution of previously altered mechanisms would significantly support their role as real biomarkers of frailty. The results showed a preponderant role of autophagy in interactome control at both different functional points, modulating other essential mechanisms in the cell, such as mitochondrial capacity or oxidative stress. Thus, the overweight provoked in the muscle of the elderly an overload of autophagy that kept cell survival in apparently healthy individuals. This excessive and permanent autophagic effort did not seem to be able to be maintained over time. Indeed, in dependent elderly, the muscle showed a total autophagic inactivity, with devastating effects on the survival of the cell, which showed clear signs of apoptosis, and reduced functional capacity. The frail elderly are in a situation of weakness that is a precursor of dependence that can still be prevented if detection is early. Hence biomarkers are essential in this context.

Indexed as

autophagybiomarkersdependencefrailtyinteractomesarcopeniaskeletal muscle

Identifiers

PMID34926470
PMCPMC8675940
OpenAlexW4200001886

What OpenQuestion holds

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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.