Evidence map›Paper›PMID 41125676›Full record

ArticleScientific reports2025

Tofogliflozin ameliorates cardiotoxin induced skeletal muscle injury and fibrosis in obesity.

Muhammad Bilal, Nguyen Quynh Phuong, Tomonobu Kado, Jianhui Liu, Le Duc Anh, Sana Khalid, Muhammad Rahil Aslam, Memoona, Ayumi Nishimura, Yoshiko Igarashi and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  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

23 authors.

Muhammad BilalFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan. drbilal@med.u-toyama.ac.jp.
Nguyen Quynh PhuongFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Tomonobu KadoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Jianhui LiuFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Le Duc AnhFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Sana KhalidDepartment of Molecular Neuroscience, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Muhammad Rahil AslamFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
MemoonaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Ayumi NishimuraFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Yoshiko IgarashiFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Yoshiyuki WatanabeFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Waseem AbbasResearch Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, 930-0194, Japan.
Maki YokoyamaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Yasuhiro OnogiResearch Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, 930-0194, Japan.
Kenichi HirabayashiDepartment of Diagnostic Pathology, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Seiji YamamotoDepartment of Pathology, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Kunimasa YagiFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Marsel LinoSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Isao UsuiDepartment of Endocrinology and Metabolism, Dokkyo Medical University, Tochigi, Japan.
Masaru KatoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Shiho FujisakaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Allah NawazFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan.
Kazuyuki TobeResearch Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, 930-0194, Japan. tobe@med.u-toyama.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity impairs muscle function through effects on lipid metabolism, systemic inflammation, and insulin resistance, leading to muscle loss and reduced regeneration. Tofogliflozin (Tofo), a sodium-glucose cotransporter 2 inhibitor (SGLT2i), exclusively inhibits SGLT2 and is used to treat hyperglycemia in patients with diabetes. The mechanism by which Tofo promotes myogenic potential in an injury model remains elusive. This study investigated Tofo's role in skeletal muscle repair in diet-induced obesity. C57BL/6 J male mice were fed a high-fat diet (HFD) with or without Tofo for 12 weeks. Cardiotoxin (CTX) was used to induce acute injury. We showed that Tofo administration during HFD alleviates obesity-induced disruption in glucose metabolism and upregulates Pax7 and MyoG expression in skeletal muscle, thereby promoting myogenesis following acute injury. Tofo activates fibro-adipogenic progenitors (FAPs) in skeletal muscle, leading to upregulated follistatin (Fst) expression and boosting the recovery process after acute injury. Mechanistically, Tofo prevented the obesity-induced decline in AMPK phosphorylation, rescued the impairment of lipid metabolism, and improved skeletal muscle function, which led to increased exercise tolerance, activation of FAPs, facilitation of skeletal muscle repair, and reduction of fibrosis.

Indexed as

Benzhydryl CompoundsCardiotoxinsGlucosidesMuscle, SkeletalObesitySodium-Glucose Transporter 2 InhibitorsAnimalsDiet, High-FatFibrosisLipid MetabolismMaleMiceMice, Inbred C57BLMuscle Development6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triolBenzhydryl CompoundsCardiotoxinsGlucosidesSodium-Glucose Transporter 2 InhibitorsCardiotoxin-induced injuryExercise toleranceFibro-adipogenic progenitors (FAPs)FollistatinSkeletal muscle

Identifiers

PMID41125676
PMCPMC12546889

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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.