Evidence map›Paper›PMID 31466311›Full record

ArticleCancers2019

Human Cachexia Induces Changes in Mitochondria, Autophagy and Apoptosis in the Skeletal Muscle.

Gabriela S de Castro, Estefania Simoes, Joanna D C C Lima, Milene Ortiz-Silva, William T Festuccia, Flávio Tokeshi, Paulo S Alcântara, José P Otoch, Dario Coletti, Marilia Seelaender

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 111 citations in OpenAlex.

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  8. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
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  20. Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024
    Review

20 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 2 countries.

Gabriela S de CastroCancer Metabolism Research Group, Department of Cell and Tissue Biology, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil. gabriela.castro@usp.br.ORCID 0000-0002-1758-9857
Estefania SimoesCancer Metabolism Research Group, Department of Cell and Tissue Biology, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil.
Joanna D C C LimaCancer Metabolism Research Group, Department of Cell and Tissue Biology, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil.
Milene Ortiz-SilvaDepartment of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil.
William T FestucciaDepartment of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil.ORCID 0000-0003-4769-0806
Flávio TokeshiDepartment of Clinical Surgery, Faculty of Medicine, University of São Paulo, 01246-903 São Paulo, Brazil.
Paulo S AlcântaraDepartment of Clinical Surgery, Faculty of Medicine, University of São Paulo, 01246-903 São Paulo, Brazil.
José P OtochDepartment of Clinical Surgery, Faculty of Medicine, University of São Paulo, 01246-903 São Paulo, Brazil.
Dario ColettiDepartment of Biological Adaptation and Aging, B2A (CNRS UMR 8256-INSERM ERL U1164-UPMC P6), Sorbonne University, 75005 Paris, France.
Marilia SeelaenderCancer Metabolism Research Group, Department of Cell and Tissue Biology, Institute of Biomedical Sciences, University of São Paulo, 05508-900 São Paulo, Brazil.
Universidade de São Paulo · BRCentre National de la Recherche Scientifique · FR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2012/50079-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/02780-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/12508-7Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/13810-9Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/12260-8
6 · The paper itself

Abstract

Cachexia is a wasting syndrome characterized by the continuous loss of skeletal muscle mass due to imbalance between protein synthesis and degradation, which is related with poor prognosis and compromised quality of life. Dysfunctional mitochondria are associated with lower muscle strength and muscle atrophy in cancer patients, yet poorly described in human cachexia. We herein investigated mitochondrial morphology, autophagy and apoptosis in the skeletal muscle of patients with gastrointestinal cancer-associated cachexia (CC), as compared with a weight-stable cancer group (WSC). CC showed prominent weight loss and increased circulating levels of serum C-reactive protein, lower body mass index and decreased circulating hemoglobin, when compared to WSC. Electron microscopy analysis revealed an increase in intermyofibrillar mitochondrial area in CC, as compared to WSC. Relative gene expression of Fission 1, a protein related to mitochondrial fission, was increased in CC, as compared to WSC. LC3 II, autophagy-related (ATG) 5 and 7 essential proteins for autophagosome formation, presented higher content in the cachectic group. Protein levels of phosphorylated p53 (Ser46), activated caspase 8 (Asp384) and 9 (Asp315) were also increased in the skeletal muscle of CC. Overall, our results demonstrate that human cancer-associated cachexia leads to exacerbated muscle-stress response that may culminate in muscle loss, which is in part due to disruption of mitochondrial morphology, dysfunctional autophagy and increased apoptosis. To the best of our knowledge, this is the first report showing quantitative morphological alterations in skeletal muscle mitochondria in cachectic patients.

Indexed as

apoptosisautophagycancer cachexiamitochondriaskeletal muscle

Identifiers

PMID31466311
PMCPMC6770124
OpenAlexW2970862723

What OpenQuestion 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 OpenQuestion graph.