Evidence map›Paper›PMID 38963460›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2024

Targeted lipidomics uncovers oxylipin perturbations and potential circulation biomarkers in Bietti's crystalline dystrophy.

Qian Li, Cong Wang, Shengjuan Zhang, Zhongjie Fu, Xiaodong Jiao, Zibing Jin, J Fielding Hejtmancik, Huan Miao, Simeng Qi, Xiaoyan Peng

Abstract read
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In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Qian LiBeijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, No.1 Dongjiaominxiang, Dongcheng District, Beijing, 100730, China. drqianli.eye@ccmu.edu.cn.ORCID http://orcid.org/0000-0003-0613-9591
Cong WangBeijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, No.1 Dongjiaominxiang, Dongcheng District, Beijing, 100730, China.
Shengjuan ZhangHebei Eye Hospital, Xingtai, Hebei, China.
Zhongjie FuDepartment of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA.
Xiaodong JiaoOphthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
Zibing JinBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
J Fielding HejtmancikOphthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
Huan MiaoLipidALL Technologies Company Limited, Changzhou, Jiangsu, China.
Simeng QiLipidALL Technologies Company Limited, Changzhou, Jiangsu, China.
Xiaoyan PengBeijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, No.1 Dongjiaominxiang, Dongcheng District, Beijing, 100730, China. 74000041@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-4275-6856

Funding

Natural Science Foundation of Beijing Municipality 7192039
6 · The paper itself

Abstract

purposeAbnormalities in lipid metabolism have been proposed in Bietti's crystalline dystrophy (BCD). We aim to characterize the lipid profiles in a case-control study.

methodsAll participants were genetically confirmed by CYP4V2 gene sequencing and underwent chorioretinopathy evaluation by calculating the percentages of AF atrophy (PAFA). Fasting blood samples of BCD patients and controls were collected, and plasma was analyzed for routine lipid profiles. Targeted lipidomic evaluation includes long chain polyunsaturated fatty acids (LCPUFA) and associated eicosanoid metabolites.

resultsRoutine lipids profiles showed elevated plasma levels of triglyceride (P = 0.043) and low-density lipoprotein cholesterol (P = 0.024) in BCD patients. Lipidomic analysis showed significantly decreased levels of ω-3 LCPUFA including docosahexaenoic acid (DHA, 22:6, P = 0.00068) and eicosapentaenoic acid (EPA, 20:5, P = 0.0016), as well as ω-6 LCPUFA arachidonic acid (ARA, 20:4, P < 0.0001) in BCD patients. Eicosanoid metabolites, either derived from ω-3 and/ or ω-6 LCPUFAs via cyclooxygenase (COX) or lipoxygenase (LOX) pathways, including 5-HEPE, 12-HEPE, 13-HDHA, 15-HETE, 12-HETE, 5-HETE, 6k-PGF1a, PGE2, PGJ2, and TXB2, exhibited significant differences (P < 0.0001) between BCD patients and controls. Genotypes of CYP4V2, specifically the biallelic null mutations, were observed to correlate with more remarkably reduced levels of oxylipins, involving major LOX pathway metabolites including 5-HETE, 5-HEPE, 12-HEPE and LTB4.

conclusionsBCD patients demonstrated significant decreases in plasma levels of ω-3 and ω-6 LCPUFA (DHA, EPA, and ARA), as well as their downstream metabolites via the COX and LOX pathways, suggesting that these might be implicated in BCD pathogenesis and could serve as biomarkers and therapeutic targets of the disease. KEY MESSAGES: What is known BCD is a vision-threatening hereditary disease the causative gene of which is CYP4V2. Abnormalities in lipid metabolism have been proposed and demonstrated previously in BCD studies. The detailed pathogenesis remains unclear and controversial. What is new We observed prominent lipidomic alterations in the circulation when compared with age, gender, and bodymass index (BMI)-matched healthy controls. BCD patients demonstrated significant decreases in plasma levels of ω-3 and ω-6 LCPUFA (DHA, EPA, and ARA). Remarkable changes were observed in the downstream metabolites of the LCPUFA via the COX and LOX pathways. Genotypes of CYP4V2, specifically the biallelic null mutations, were observed to correlate with more remarkably reduced levels of oxylipins, involving major LOX pathway metabolites.

Indexed as

BiomarkersCorneal Dystrophies, HereditaryLipidomicsOxylipinsAdultCase-Control StudiesCytochrome P450 Family 4DNAFemaleHumansLipid MetabolismMaleMiddle AgedRetinal DiseasesBiomarkersCYP4V2 protein, humanCytochrome P450 Family 4DNAOxylipinsBietti’s crystalline dystrophyCYP4V2LipidMediatorsPUFA

Identifiers

PMID38963460

What Socratic holds

Textmetadata
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Registered trials

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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 Socratic graph.