Evidence map›Paper›PMID 41208194›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Thyroid Hormone Receptor β1 and PGC1α Coordinately Regulate OPA1/MFN2-Mediated Mitochondrial Fusion and UCP1-Mediated Lipid Browning in ccRCC.

Xiangui Meng, Tiexi Yu, Fang Lv, Weiquan Li, Hongmei Yang, Xiaoping Zhang, Wen Xiao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. 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. Article
  2. Article
  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

7 authors.

Xiangui MengDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Tiexi YuDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Fang LvDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Weiquan LiDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Hongmei YangDepartment of Pathogenic Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiaoping ZhangDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Wen XiaoDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.ORCID https://orcid.org/0000-0002-2013-7157

Funding

National Natural Science Foundation of China 81902588National Natural Science Foundation of China 82372845National Natural Science Foundation of China 82503915National Natural Science Foundation of China 82504126Science Foundation of Union Hospital 2022XHYN030Science Foundation of Union Hospital 2024XHYN045Science Foundation of Union Hospital 2024XHYN048
6 · The paper itself

Abstract

The abnormal accumulation of lipids is a hallmark of clear cell renal cell carcinoma (ccRCC). Both the thyroid hormone receptor β1 (TRβ) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) are key regulators of mitochondrial function and lipid metabolism. However, their specific interaction and influence on ccRCC development and lipid accumulation remain poorly understood. This study identified genes jointly regulated by TRβ and PGC1α, which are implicated in lipid browning and mitochondrial fusion. Mechanistically, T3-activated TRβ interacts with PGC1α to transcriptionally upregulate PGC1α, UCP1, and mitochondrial fusion genes OPA1 and MFN2, thereby enhancing mitochondrial activity, promoting lipid utilization, and suppressing ccRCC progression. These results indicate that the mitochondrial and metabolic effects of TRβ in ccRCC are mediated through PGC1α expression and function. Activation of the TRβ/PGC1α through hormonal and pharmacological means may offer a promising therapeutic approach for ccRCC.

Indexed as

GTP PhosphohydrolasesLipid MetabolismPPAR gammaThyroid Hormone Receptors betaCarcinoma, Renal CellCell Line, TumorHumansMitochondrial DynamicsMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaGTP PhosphohydrolasesMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaPPARGC1A protein, humanThyroid Hormone Receptors betaccRCClipid browningmitochondrial fusionthe peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α)the thyroid hormone receptor β1 (TRβ)

Identifiers

PMID41208194
PMCPMC12849942

What Socratic 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 Socratic graph.