Evidence map›Paper›PMID 34831373›Full record

ReviewCells2021

Mitochondrial Dysfunction in Cancer Cachexia: Impact on Muscle Health and Regeneration.

Marc Beltrà, Fabrizio Pin, Riccardo Ballarò, Paola Costelli, Fabio Penna

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.2field-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

43 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  11. Review
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  14. Hallmarks of Cancer Cachexia: Sexual Dimorphism in Related Pathways.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Article
  17. Body composition alterations in patients with lung cancer.American journal of physiology. Cell physiology · 2025
    Review
  18. Article
  19. Article
  20. Review
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 2 institutions in 2 countries.

Marc BeltràDepartment of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy.ORCID 0000-0001-6070-9861
Fabrizio PinDepartment of Anatomy, Cell Biology and Physiology, Indiana University, Indianapolis, IN 46202, USA.
Riccardo BallaròDepartment of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy.ORCID 0000-0001-5505-9024
Paola CostelliDepartment of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy.
Fabio PennaDepartment of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy.ORCID 0000-0002-2774-6027
University of Turin · ITIndiana University – Purdue University Indianapolis · US

Funding

Associazione Italiana per la Ricerca sul Cancro IG 2018-ID. 21963
6 · The paper itself

Abstract

Cancer cachexia is a frequently neglected debilitating syndrome that, beyond representing a primary cause of death and cancer therapy failure, negatively impacts on patients' quality of life. Given the complexity of its multisystemic pathogenesis, affecting several organs beyond the skeletal muscle, defining an effective therapeutic approach has failed so far. Revamped attention of the scientific community working on cancer cachexia has focused on mitochondrial alterations occurring in the skeletal muscle as potential triggers of the complex metabolic derangements, eventually leading to hypercatabolism and tissue wasting. Mitochondrial dysfunction may be simplistically viewed as a cause of energy failure, thus inducing protein catabolism as a compensatory mechanism; however, other peculiar cachexia features may depend on mitochondria. On the one side, chemotherapy also impacts on muscle mitochondrial function while, on the other side, muscle-impaired regeneration may result from insufficient energy production from damaged mitochondria. Boosting mitochondrial function could thus improve the energetic status and chemotherapy tolerance, and relieve the myogenic process in cancer cachexia. In the present work, a focused review of the available literature on mitochondrial dysfunction in cancer cachexia is presented along with preliminary data dissecting the potential role of stimulating mitochondrial biogenesis via PGC-1α overexpression in distinct aspects of cancer-induced muscle wasting.

Indexed as

RegenerationAnimalsCachexiaHumansMitochondriaMuscle DevelopmentMusclesNeoplasmscancer cachexiametabolismmitochondriamuscle wastingmyogenesisPGC-1αregeneration

Identifiers

PMID34831373
PMCPMC8621344
OpenAlexW3214322290

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.