Evidence map›Paper›PMID 41165841›Full record

ArticleCellular and molecular life sciences : CMLS2025

SIRT7 drives energy metabolic shifts in endometriosis via interaction with TUFM and Rhoa/Rock/Akt pathway activation.

Huaying Zhang, Jiahao Chen, Mengjie Yang, Xinyu Ding, Guolin Chai, Ruofan Huang, Dianchao Lin, Zhixiong Huang, Qionghua Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Research Progress of Histone Deacetylase and Its Inhibitors in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  2. Review
  3. Article
  4. 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

9 authors.

Huaying ZhangClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Jiahao ChenClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Mengjie YangClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Xinyu DingClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Guolin ChaiClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Ruofan HuangClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Dianchao LinClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Zhixiong HuangClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China. zhixiong0815@163.com.
Qionghua ChenClinical MedicalResearch Center for Gynecological Reproductive Health of Fujian Province, Laboratory ofResearch and Diagnosis of Gynecological Diseases of Xiamen City, Department ofObstetrics and Gynecology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China. cqhua616@126.com.ORCID http://orcid.org/0000-0003-4637-9813

Funding

National Natural Science Foundation of China 82171638National Natural Science Foundation of China 82271678National Natural Science Foundation of China 82301852
6 · The paper itself

Abstract

purposeEndometriosis is characterized by the ectopic growth of endometrial-like tissue outside the uterus and altered energy metabolism, but the specific mechanisms involved remain unclear. This study aimed to investigate the impact of Sirtuins7 (SIRT7) on metabolic homeostasis to better understand the metabolic alterations underlying endometriosis.

methodsIntegrated metabolomic, transcriptomic, and proteomic analyses revealed metabolic dysregulation in endometriosis. Seahorse XF technology was used to assess metabolic rates. The effects of SIRT7 on endometriosis were validated both in vitro and in vivo. Immunoprecipitation and mass spectrometry were used to identify the interaction between SIRT7 and Tu translation elongation factor, mitochondrial (TUFM). Cellular phenotypes, including proliferation, migration, and apoptosis, were evaluated by CCK-8 assays, Transwell and scratch assays, and flow cytometry.

resultsMultiomics analyses and Seahorse XF tests revealed a metabolic shift from mitochondrial respiration to glycolysis in ectopic tissues. SIRT7 was found to be upregulated in ectopic lesions and significantly influenced the progression of endometriosis. In addition, an interaction between SIRT7 and TUFM has been observed. The metabolic reprogramming, proliferation and migration ability of endometrial stromal cells were greatly reduced by SIRT7 knockdown and TUFM overexpression. The effects of TUFM deficiency were reversed by SIRT7 knockdown. The results also demonstrated that SIRT7 promoted the glycolytic enzymes GBE1 and PYGL, suppressed the mitochondrial enzymes IDH1 and SDHB, and activated the RhoA/ROCK/AKT pathway and the EMT process, thereby facilitating the progression of endometriosis.

conclusionsThese findings underscore the critical involvement of SIRT7 in the energy metabolism reprogramming of ectopic cells. Our research provides valuable insights for the development of nonsurgical treatment strategies for endometriosis.

Indexed as

EndometriosisEnergy MetabolismProto-Oncogene Proteins c-aktrhoA GTP-Binding ProteinSirtuinsAnimalsApoptosisCell MovementCell ProliferationEndometriumFemaleGlycolysisHumansMiceMitochondriaSignal TransductionProto-Oncogene Proteins c-aktrhoA GTP-Binding ProteinRHOA protein, humanSIRT7 protein, humanSirtuinsEndometriosisMetabolic reprogrammingMigrationProliferationSIRT7TUFM

Identifiers

PMID41165841
PMCPMC12575906

What Socratic holds

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LicenceCC BY-NC-ND
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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.