Evidence map›Paper›PMID 41963969›Full record

ArticleBMC complementary medicine and therapies2026

Elucidating the vasoprotective mechanism of Tetrahydrocurcumin: from unbiased transcriptomic discovery to targeted validation of the PI3K/AKT pathway.

Yi-Lin Chiu, Tsai-Jung Lin, Hsing-Fan Lai, Yu-Sin Chang, Tzu-Chiao Lin, Yen-Lien Chou, Cheng-Chung Cheng, Sharon Fong, Tsung-Neng Tsai

Abstract read
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In one paragraph

Article in BMC complementary medicine and therapies, 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
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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

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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

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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.

Yi-Lin Chiu *Graduate Institute of Biochemistry, College of Biomedical Sciences, National Defense Medical University, Taipei, Taiwan, ROC.
Tsai-Jung Lin *Division of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Hsing-Fan LaiGraduate Institute of Life Sciences, College of Biomedical Sciences, National Defense Medical University, Taipei, Taiwan, ROC.
Yu-Sin ChangGraduate Institute of Biochemistry, College of Biomedical Sciences, National Defense Medical University, Taipei, Taiwan, ROC.
Tzu-Chiao LinDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Yen-Lien ChouDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Cheng-Chung ChengDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Sharon FongDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC.
Tsung-Neng TsaiDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical University, Number 325, Section 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, ROC. genetic2001@hotmail.com.

Funding

Medical Affairs Bureau MND-MAB-C09-113033Medical Affairs Bureau MND-MAB-D-114166National Science and Technology Council NSTC-111-2314-B-016-019-MY3National Science and Technology Council NSTC-113-2314-B-016-020Tri-Service General Hospital TSGH-D-112047
6 · The paper itself

Abstract

Endothelial dysfunction is a critical initiating event in atherosclerosis. Endothelial nitric oxide synthase (eNOS) plays a key role in maintaining vascular health by producing nitric oxide (NO) to regulate vascular tone. Tetrahydrocurcumin (THCu), a stable metabolite of curcumin, exhibits promising bioactivity; however, its precise vasoprotective mechanism remains unclear. This study investigated the hypothesis that THCu enhances eNOS function in human umbilical vein endothelial cells by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Our results demonstrate that THCu treatment robustly and dose-dependently increased PI3K and AKT phosphorylation. This upstream activation directly led to eNOS phosphorylation at Ser1177, significantly boosting NO bioavailability. Pharmacological inhibition of PI3K or AKT completely abolished THCu-induced eNOS phosphorylation and NO release. In conclusion, this research delineates a clear mechanistic framework establishing the PI3K/AKT cascade as the essential pathway for THCu-mediated eNOS activation, providing a strong scientific rationale for its further investigation as a candidate for mitigating endothelial dysfunction in atherosclerosis.

Indexed as

CurcuminNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAtherosclerosisHumansHuman Umbilical Vein Endothelial CellsNitric OxidePhosphorylationSignal TransductionCurcuminNitric OxideNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akttetrahydrocurcuminAtherosclerosisEndothelial cellseNOSMachine learningPI3K/AKT pathwayTetrahydrocurcuminTranscriptomics

Identifiers

PMID41963969
PMCPMC13203002

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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.