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Metabolites
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Metabolomics of Heart Failure and Its Comorbidities
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Metabolomics of Heart Failure and Its Comorbidities

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 6086

Special Issue Editor

Prof. Dr. Bing Yu

E-Mail Website
Guest Editor
Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA
Interests: big data; data science; epidemiology; genetics; omics; women's health; cardiovascular; chronic diseases

Special Issue Information

Dear Colleagues,

Heart failure is a complex clinical syndrome, which results from disorders that impair ventricular filling or ejection of blood. Despite advances in treatment, the prognosis of heart failure remains poor. An intrinsic component of heart failure pathophysiology is the impairment of cardiac function. Metabolic dysfunction, such as impaired branched-chain amino acid catabolism, decreased fatty acid oxidation, and depressed urea cycle function, are detectable in at-risk individuals prior to the development of heart failure and may contribute to alterations in cardiac structure and function. Comorbidities frequently accompany heart failure—for example, hypertension, diabetes, and hyperlipidemia, which are also affected by metabolic dysfunction. The role of metabolic dysfunction in the progression of cardiac dysfunction and its relationship to heart failure incidence, as well as its interplay with comorbidities, remain elusive. This Special Issue of Metabolites will be dedicated to publishing current advances in metabolic changes that contribute to cardiac dysfunction, heart failure, and its comorbidities.

Prof. Dr. Bing Yu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hypertension
  • diabetes
  • coronary heart disease
  • atrial fibrillation
  • metabolic syndrome
  • cardiac dysfunction
  • systemic inflammation

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Published Papers (2 papers)

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Research

11 pages, 22861 KiB  
Article
Metabolite Signature of Simvastatin Treatment Involves Multiple Metabolic Pathways
by Lilian Fernandes Silva, Rowmika Ravi, Jagadish Vangipurapu and Markku Laakso
Metabolites 2022, 12(8), 753; https://doi.org/10.3390/metabo12080753 - 16 Aug 2022
Cited by 7 | Viewed by 2213
Abstract
Statins inhibit the 3-hydroxy-3-methylglutaryl-CoA reductase enzyme and are the most widely used medication for hypercholesterolemia. Previous studies on the metabolite signature of simvastatin treatment have included only a small number of metabolites. We performed a high-throughput liquid chromatography–tandem mass spectroscopy profiling on the [...] Read more.
Statins inhibit the 3-hydroxy-3-methylglutaryl-CoA reductase enzyme and are the most widely used medication for hypercholesterolemia. Previous studies on the metabolite signature of simvastatin treatment have included only a small number of metabolites. We performed a high-throughput liquid chromatography–tandem mass spectroscopy profiling on the effects of simvastatin treatment on 1098 metabolite concentrations in the participants of the METSIM (Metabolic Syndrome In Men) study including 1332 participants with simvastatin treatment and 6200 participants without statin treatment. We found that simvastatin exerts profound pleiotropic effects on different metabolite pathways, affecting not only lipids, but also amino acids, peptides, nucleotides, carbohydrates, co-factors, vitamins, and xenobiotics. We identified 321 metabolites significantly associated with simvastatin treatment, and 313 of these metabolites were novel. Our study is the first comprehensive evaluation of the metabolic signature of simvastatin treatment in a large population-based study. Full article
(This article belongs to the Special Issue Metabolomics of Heart Failure and Its Comorbidities)
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14 pages, 1461 KiB  
Article
Cross-Sectional Blood Metabolite Markers of Hypertension: A Multicohort Analysis of 44,306 Individuals from the COnsortium of METabolomics Studies
by Panayiotis Louca, Ana Nogal, Aurélie Moskal, Neil J. Goulding, Martin J. Shipley, Taryn Alkis, Joni V. Lindbohm, Jie Hu, Domagoj Kifer, Ni Wang, Bo Chawes, Kathryn M. Rexrode, Yoav Ben-Shlomo, Mika Kivimaki, Rachel A. Murphy, Bing Yu, Marc J. Gunter, Karsten Suhre, Deborah A. Lawlor, Massimo Mangino and Cristina Menniadd Show full author list remove Hide full author list
Metabolites 2022, 12(7), 601; https://doi.org/10.3390/metabo12070601 - 28 Jun 2022
Cited by 12 | Viewed by 3222
Abstract
Hypertension is the main modifiable risk factor for cardiovascular morbidity and mortality but discovering molecular mechanisms for targeted treatment has been challenging. Here we investigate associations of blood metabolite markers with hypertension by integrating data from nine intercontinental cohorts from the COnsortium of [...] Read more.
Hypertension is the main modifiable risk factor for cardiovascular morbidity and mortality but discovering molecular mechanisms for targeted treatment has been challenging. Here we investigate associations of blood metabolite markers with hypertension by integrating data from nine intercontinental cohorts from the COnsortium of METabolomics Studies. We included 44,306 individuals with circulating metabolites (up to 813). Metabolites were aligned and inverse normalised to allow intra-platform comparison. Logistic models adjusting for covariates were performed in each cohort and results were combined using random-effect inverse-variance meta-analyses adjusting for multiple testing. We further conducted canonical pathway analysis to investigate the pathways underlying the hypertension-associated metabolites. In 12,479 hypertensive cases and 31,827 controls without renal impairment, we identified 38 metabolites, associated with hypertension after adjusting for age, sex, body mass index, ethnicity, and multiple testing. Of these, 32 metabolite associations, predominantly lipid (steroids and fatty acyls) and organic acids (amino-, hydroxy-, and keto-acids) remained after further adjusting for comorbidities and dietary intake. Among the identified metabolites, 5 were novel, including 2 bile acids, 2 glycerophospholipids, and ketoleucine. Pathway analysis further implicates the role of the amino-acids, serine/glycine, and bile acids in hypertension regulation. In the largest cross-sectional hypertension-metabolomics study to date, we identify 32 circulating metabolites (of which 5 novel and 27 confirmed) that are potentially actionable targets for intervention. Further in-vivo studies are needed to identify their specific role in the aetiology or progression of hypertension. Full article
(This article belongs to the Special Issue Metabolomics of Heart Failure and Its Comorbidities)
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