Evidence map›Paper›PMID 39877365›Full record

ArticleFrontiers in immunology2024

Fatty acid synthase inhibition improves hypertension-induced erectile dysfunction by suppressing oxidative stress and NLRP3 inflammasome-dependent pyroptosis through activating the Nrf2/HO-1 pathway.

Jiaochen Luan, Mengchi Yu, Qi Gu, Xuan Zhou, Yunqiang Shao, Tong Chen, Jiayi Zhang, Zheng Zhu, Ninghong Song, Jie Yang

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

10 authors.

Jiaochen Luan *Department of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mengchi Yu *Department of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qi Gu *Department of Urology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Xuan Zhou *Department of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yunqiang ShaoDepartment of Urology, People's Hospital of Xinjiang Kizilsu Kirgiz Autonomous Prefecture, Kizilsu Kirgiz Autonomous Prefecture, China.
Tong ChenDepartment of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiayi ZhangDepartment of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zheng ZhuDepartment of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ninghong SongDepartment of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jie YangDepartment of Urology, Jiangsu Provincial People's Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Erectile dysfunction (ED) is a prevalent male sexual disorder, commonly associated with hypertension, though the underlying mechanisms remain poorly understood. Objective: This study aims to explore the role of Fatty acid synthase (Fasn) in hypertension-induced ED and evaluate the therapeutic potential of the Fasn inhibitor C75. Materials and methods: Erectile function was assessed by determining the intracavernous pressure/mean arterial pressure (ICP/MAP) ratio, followed by the collection of cavernous tissue for transcriptomic and non-targeted metabolomic analyses. Results: The SHR exhibited ED, indicated by reduced maximum ICP/MAP ratios. Histologically, corpus cavernosum tissue of SHR showed elevated fibrosis and endothelial dysfunction. Additionally, increased expression of the NLRP3 inflammasome, Caspase-1, GSDMD, and the pro-inflammatory cytokines IL-1β and IL-18 was observed. Multi-omics analysis revealed significant enrichment in lipid metabolic pathways, with Fasn identified as a hub gene. Conclusion: These findings suggest that Fasn inhibition may offer a promising therapeutic strategy for hypertension-induced ED by alleviating oxidative stress and suppressing NLRP3 inflammasome-dependent endothelial cell pyroptosis

Indexed as

Erectile DysfunctionFatty Acid SynthasesHypertensionInflammasomesNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressPyroptosis4-ButyrolactoneAnimalsDisease Models, AnimalHeme Oxygenase-1Heme Oxygenase (Decyclizing)MaleRatsRats, Inbred SHR4-Butyrolactone4-methylene-2-octyl-5-oxofuran-3-carboxylic acidFatty Acid SynthasesHeme Oxygenase-1Heme Oxygenase (Decyclizing)Hmox1 protein, ratInflammasomesNfe2l2 protein, ratNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, raterectile dysfunctionFasnhypertensionNrf2/HO-1pyroptosis

Identifiers

PMID39877365
PMCPMC11772187

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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.