Serum Metabonomic Study of Patients With Acute Coronary Syndrome Using Ultra-Performance Liquid Chromatography Orbitrap Mass Spectrometer

Song, Lei; Zhang, Zhongxiao; Qiu, Zhaohui; Jiang, Tingbo

doi:10.3389/fcvm.2021.637621

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…Other diseases such as hypertension ( 33 ) and ischemic injury ( 34 ) also provoke inflammatory responses, leading to cardiac hypertrophy. TLRs are widely expressed in many cells in the heart, and activating TLR-mediated inflammation signaling pathways promotes immune cell migration to the heart and cardiac fibroblast differentiation ( 35 , 36 ). Therefore, TLR-induced inflammatory signaling is significant in the development of cardiac hypertrophy.…”

Section: Inflammation Is Involved In the Pathogenesis Of Cardiac Hype...mentioning

confidence: 99%

Toll-like receptors in cardiac hypertrophy

Zhang

Dong

et al. 2023

Front. Cardiovasc. Med.

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Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRRs) that can identify pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). TLRs play an important role in the innate immune response, leading to acute and chronic inflammation. Cardiac hypertrophy, an important cardiac remodeling phenotype during cardiovascular disease, contributes to the development of heart failure. In previous decades, many studies have reported that TLR-mediated inflammation was involved in the induction of myocardium hypertrophic remodeling, suggesting that targeting TLR signaling might be an effective strategy against pathological cardiac hypertrophy. Thus, it is necessary to study the mechanisms underlying TLR functions in cardiac hypertrophy. In this review, we summarized key findings of TLR signaling in cardiac hypertrophy.

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Section: Inflammation Is Involved In the Pathogenesis Of Cardiac Hype...mentioning

confidence: 99%

Toll-like receptors in cardiac hypertrophy

Zhang

Dong

et al. 2023

Front. Cardiovasc. Med.

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“…The content of L-carnitine and ATP in ischemic myocardium is significantly reduced, and free fatty acids are increased, leading to disturbances in myocardial cell energy metabolism [ 22 ]. Myocardial L-carnitine levels are significantly reduced, while blood L-carnitine levels are elevated, resulting from myocardial ischemia leading to partial release of L-carnitine into the blood or blocked transport of L-carnitine into cardiac myocytes [ 23 ]. Joanna et al .…”

Section: Application Of Metabolomics In Acsmentioning

confidence: 99%

Progress in the Metabolomics of Acute Coronary Syndrome

Fu¹,

Li²,

Su³

et al. 2023

Rev. Cardiovasc. Med.

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Acute coronary syndrome (ACS) is a severe type of coronary heart disease (CHD) with increasing prevalence and significant challenges for prevention and treatment. Metabolomics is an emerging technology with intrinsic dynamics and flexibility to better delineate the phenotypic and metabolic alterations in organisms at the time of altered pathological states. It provides new insights into the complex pathological mechanisms of cardiovascular disease and contributes to the early detection, monitoring and evaluation of ACS. In this review, we analyze and summarize the literature related to ACS metabolomics which has contributed to the diagnosis and prevention of ACS.

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“…Metabolomics is an emerging discipline that quantifies the low-molecular-weight metabolites of an organism or cell [ 5 ]. It is extensively used to diagnose a variety of diseases, such as CNS disorders.…”

Section: Introductionmentioning

confidence: 99%

Untargeted Metabolomic Profiling of Cuprizone‐Induced Demyelination in Mouse Corpus Callosum by UPLC‐Orbitrap/MS Reveals Potential Metabolic Biomarkers of CNS Demyelination Disorders

Zhao

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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Multiple sclerosis (MS) is a neurodegenerative disorder characterized by periodic neuronal demyelination, which leads to a range of symptoms and eventually to disability. The goal of this research was to use UPLC-Orbitrap/MS to identify validated biomarkers and explore the metabolic mechanisms of MS in mice. Thirty-two C57BL/6 male mice were randomized into two groups that were fed either normal food or 0.2% CPZ for 11 weeks. The mouse demyelination model was assessed by LFB and the expression of MBP by immunofluorescence and immunohistochemistry. The metabolites of the corpus callosum were quantified using UPLC-Orbitrap/MS. The mouse pole climbing experiment was used to assess coordination ability. Multivariate statistical analysis was adopted for screening differential metabolites, and the ingenuity pathway analysis (IPA) was used to reveal the metabolite interaction network. We successfully established the demyelination model. The CPZ group slowly lost weight and showed an increased pole climbing time during feeding compared to the CON group. A total of 81 metabolites ( VIP > 1 and P < 0.05 ) were determined to be enriched in 24 metabolic pathways; 41 metabolites were markedly increased, while 40 metabolites were markedly decreased in the CPZ group. The IPA results revealed that these 81 biomarker metabolites were associated with neuregulin signaling, PI3K-AKT signaling, mTOR signaling, and ERK/MAPK signaling. KEGG pathway analysis showed that two significantly different metabolic pathways were enriched, namely, the glycerophospholipid and sphingolipid metabolic pathways, comprising a total of nine biomarkers. Receiver operating characteristic analysis showed that the metabolites (e.g., PE (16 : 0/22 : 6(4Z, 7Z, 10Z, 13Z, 16Z, 19Z)), PC (18 : 0/22 : 4(7Z, 10Z, 13Z, 16Z)), cytidine 5 ′ -diphosphocholine, PS (18 : 0/22 : 6(4Z, 7Z, 10Z, 13Z, 16Z, 19Z)), glycerol 3-phosphate, SM (d18 : 0/16 : 1(9Z)), Cer (d18:1/18 : 0), galabiosylceramide (d18:1/18 : 0), and GlcCer (d18:1/18 : 0)) have good discrimination ability for the CPZ group. In conclusion, the differential metabolites have great potential to serve as biomarkers of demyelinating diseases. In addition, we identified metabolic pathways associated with CPZ-induced demyelination pathogenesis, which provided a new perspective for understanding the relationship between metabolites and CNS demyelination pathogenesis.

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Serum Metabonomic Study of Patients With Acute Coronary Syndrome Using Ultra-Performance Liquid Chromatography Orbitrap Mass Spectrometer

Cited by 6 publications

References 32 publications

Toll-like receptors in cardiac hypertrophy

Toll-like receptors in cardiac hypertrophy

Progress in the Metabolomics of Acute Coronary Syndrome

Untargeted Metabolomic Profiling of Cuprizone‐Induced Demyelination in Mouse Corpus Callosum by UPLC‐Orbitrap/MS Reveals Potential Metabolic Biomarkers of CNS Demyelination Disorders

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