Evidence map›Paper›PMID 42841610›Full record

ArticleAging cell2026

Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.

Hamsa Vardini Senthil Kumar, Debanik Choudhury, Pedro Lei, Pihu Mehrotra, Shahryar Shahini, Sydney Swedick, John Toftegaard, Stelios T Andreadis

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Hamsa Vardini Senthil KumarGenetics Genomics and Bioinformatics Program, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0009-0006-2080-821X
Debanik ChoudhuryDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0009-0002-1987-1749
Pedro LeiDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0000-0002-3550-8715
Pihu MehrotraDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0000-0001-9369-5013
Shahryar ShahiniDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0000-0003-3813-6424
Sydney SwedickDepartment of Biomedical Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0009-0008-7061-8777
John ToftegaardDepartment of Biomedical Engineering, University at Buffalo, Buffalo, New York, USA.
Stelios T AndreadisDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, New York, USA.ORCID https://orcid.org/0000-0001-9885-0457

Funding

Restoring the regenerative capacity of the aged muscleR01AG068250 · NIA · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI ANDREADIS, STELIOS THEOHARIS · 2020 to 2024
$2.0M
NIA NIH HHS R01 AG068250
6 · The paper itself

Abstract

Age-associated loss of skeletal muscle mass and function, also known as sarcopenia, is closely linked to mitochondrial dysfunction. In this study, we report that senescent skeletal muscle myoblasts exhibit elevated activity and expression of the enzyme glutaminase (GLS1), which is mediated by p38 MAPK signaling and leads to intracellular urea accumulation that impairs mitochondrial function. Pharmacological inhibition of GLS1 with CB-839 reduced urea levels, restored the expression of electron transport chain (ETC) complexes, and improved mitochondrial function. Consistent with our in vitro findings, CB-839 administration to progeroid mice similarly upregulated ETC complexes and enhanced mitochondrial respiratory capacity in skeletal muscle, leading to improved structural integrity and enhanced muscle strength. Together, these findings suggest that targeting glutamine metabolism via GLS1 inhibition may represent a promising therapeutic strategy to ameliorate age-related skeletal muscle decline by restoring mitochondrial health.

Indexed as

Cellular SenescenceGlutaminaseMitochondriaMitochondria, MuscleMuscle, SkeletalSarcopeniaAgingAnimalsMicep38 Mitogen-Activated Protein KinasesGlutaminasep38 Mitogen-Activated Protein Kinases

Identifiers

PMID42841610
PMCPMC13644385

What OpenQuestion holds

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Registered trials

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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.