Spatially Resolved Metabolites in Stable and Unstable Human Atherosclerotic Plaques Identified by Mass Spectrometry Imaging.
Spatially Resolved Metabolites in Stable and Unstable Human Atherosclerotic Plaques Identified by Mass Spectrometry Imaging.
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通过质谱成像鉴定稳定和不稳定的人类动脉粥样硬化斑块中的空间分辨代谢物。
DOI：
10.1161/atvbaha.122.318684
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Pattillo,Chr
中科院分区：
文献类型：
--
作者：
Seeley,ErinH;Liu,Zhipeng;Yuan,Shuai;Stroope,Chad;Cockerham,Elizabeth;Rashdan,NabilA;Delgadillo,LuisaF;Finney,AlexandraC;Kumar,Dhananjay;Das,Sandeep;Razani,Babak;Liu,Wanqing;Traylor,James;Orr,AWayne;Rom,Oren;Pattillo,Chr
BackgroundImpairments in carbohydrate, lipid, and amino acid metabolism drive features of plaque instability. However, where these impairments occur within the atheroma remains largely unknown. Therefore, we sought to characterize the spatial distribution of metabolites within stable and unstable atherosclerosis in both the fibrous cap and necrotic core.MethodsAtherosclerotic tissue specimens from 9 unmatched individuals were scored based on the Stary classification scale and subdivided into stable and unstable atheromas. After performing mass spectrometry imaging on these samples, we identified over 850 metabolite-related peaks. Using MetaboScape, METASPACE, and Human Metabolome Database, we confidently annotated 170 of these metabolites and found over 60 of these were different between stable and unstable atheromas. We then integrated these results with an RNA-sequencing data set comparing stable and unstable human atherosclerosis.ResultsUpon integrating our mass spectrometry imaging results with the RNA-sequencing data set, we discovered that pathways related to lipid metabolism and long-chain fatty acids were enriched in stable plaques, whereas reactive oxygen species, aromatic amino acid, and tryptophan metabolism were increased in unstable plaques. In addition, acylcarnitines and acylglycines were increased in stable plaques whereas tryptophan metabolites were enriched in unstable plaques. Evaluating spatial differences in stable plaques revealed lactic acid in the necrotic core, whereas pyruvic acid was elevated in the fibrous cap. In unstable plaques, 5-hydroxyindoleacetic acid was enriched in the fibrous cap.ConclusionsOur work here represents the first step to defining an atlas of metabolic pathways involved in plaque destabilization in human atherosclerosis. We anticipate this will be a valuable resource and open new avenues of research in cardiovascular disease.
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