Evidence map›Paper›PMID 40790174›Full record

ArticleBMC cancer2025

Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females.

Francielly Morena, Seongkyun Lim, Ana Regina Cabrera, Toby L Chambers, Pieter J Koopmans, Stavroula Tsitkanou, Sabin Khadgi, Calvin Peterson, Eleanor R Schrems, Ruqaiza Muhyudin and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

16 authors.

Francielly MorenaDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Seongkyun LimDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Ana Regina CabreraDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Toby L ChambersDepartment of Health, Human Performance and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Pieter J KoopmansDepartment of Health, Human Performance and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Stavroula TsitkanouDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Sabin KhadgiDepartment of Health, Human Performance and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Calvin PetersonDepartment of Health, Human Performance and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Eleanor R SchremsDepartment of Health, Human Performance and Recreation, Exercise Muscle Biology Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Ruqaiza MuhyudinDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Sepideh ShakeriDepartment of Health, Human Performance and Recreation, Exercise Muscle Biology Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Kevin ZhaoDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Devan MishraDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA.
Tyrone A WashingtonDepartment of Health, Human Performance and Recreation, Exercise Muscle Biology Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Kevin A MurachDepartment of Health, Human Performance and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, AR, USA.
Nicholas P GreeneDepartment of Health, Human Performance and Recreation, Cachexia Research Laboratory, Exercise Science Research Center, University of Arkansas, 155 Stadium Dr., Fayetteville, AR, 72701, USA. npgreene@uark.edu.

Funding

The role of autophagy in bone remodelingP20GM125503 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · 2023 to 2025
$6.8M
NIAMS NIH HHS 5R01AR075794NIAMS NIH HHS R01 AR075794NIGMS NIH HHS P20 GM125503NIGMS NIH HHS P20GM125503
6 · The paper itself

Abstract

backgroundSkeletal muscle atrophy during cancer-induced cachexia remains a significant challenge in cancer management. Mitochondrial defects precede muscle mass and functional losses in models of cancer cachexia (CC). We hypothesized targeting Opa1-a key regulator of mitochondrial fusion-can attenuate LLC-induced CC outcomes.

methodsWe utilized 1) in vivo transgenic Opa1 overexpression (OPA1 TG) in LLC-induced CC in vivo, and 2) BPG15 administration to induce Opa1 in vitro and in vivo.

resultsOPA1 TG attenuated plantaris, gastrocnemius, and EDL loss with LLC in males and alleviated gastrocnemius loss in females. OPA1 TG had greater mitochondrial respiration in plantaris and white gastrocnemius, and lowered pMitoTimer Red Puncta (-63%), a proxy for mitophagy in males. OPA1 TG protected muscle contractility at physiological stimulation frequencies by up to 60% in female LLC mice. OPA1 TG enhanced the ratio of OPA1/DRP1 protein content-a proxy for fusion and fission balance-in males and females. In vitro, BGP-15 attenuated LLC conditioned media-induced myotube atrophy by ~ 9% concomitant with suppression of the transcriptional factor FoxO3, autophagy markers, and inflammatory cytokines. In vivo, BGP-15 improved contractility at lower frequencies (10-60 Hz), with LLC-BGP-15 showing up to 20% greater torque than LLC-control. BGP-15 treated LLC animals had 71% fewer pMitoTimer red puncta, suggesting attenuated mitophagy.

conclusionsPromoting mitochondrial fusion via OPA1 induction improved cachectic outcomes in mice. Targeting OPA1providing provides a promising therapeutic approach for CC treatment.

Indexed as

CachexiaGTP PhosphohydrolasesMitochondrial DynamicsMuscular AtrophyNeoplasmsAnimalsDisease Models, AnimalFemaleForkhead Box Protein O3HumansMaleMiceMice, TransgenicMitochondriaMitophagyMuscle, SkeletalForkhead Box Protein O3GTP PhosphohydrolasesOpa1 protein, mouseBGP-15Lewis Lung CarcinomaMitochondrial dynamicsMuscle contractilityOPA1

Identifiers

PMID40790174
PMCPMC12337443

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.