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IJMS
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Molecular Mechanisms Linking Obesity to Atherosclerosis Pathogenesis
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Molecular Mechanisms Linking Obesity to Atherosclerosis Pathogenesis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 July 2025 | Viewed by 31

Special Issue Editor

Prof. Dr. Weibin Shi

E-Mail Website
Guest Editor
Departments of Radiology and Medical Imaging and of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA
Interests: atherosclerosis; lipid metabolism; type 2 diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is a major risk factor for atherosclerosis and its complications. Most observation studies show that obesity is independently associated with the prevalence, extent, and severity of coronary artery disease. Obesity is also independently associated with type 2 diabetes, hypertension, and dyslipidemia, all of which are major risk factors for atherosclerosis. Many observations have suggested a complex relationship between obesity and cardiovascular disease. 

In this Special Issue, we welcome the submission of both original and review articles that explore the complex relationship between obesity and atherosclerosis at the molecular and cellular levels. All aspects of molecular and cellular biology, pathology, and molecular medicine exploring the mechanisms, potential treatments, and impact of obesity on atherosclerosis fit the scope of IJMS. We will also consider studies that reveal the molecular, cellular, and biochemical mechanisms of atherogenesis in obese patients. Among the mechanisms to be studied are lipid metabolism, innate immunity, chronic inflammation, and oxidative stress.

We look forward to receiving your contributions.

Prof. Dr. Weibin Shi
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • obesity
  • overweight
  • atherosclerosis
  • coronary artery disease
  • obesity paradox
  • body mass index
  • visceral fat

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Published Papers (1 paper)

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Research

19 pages, 2205 KiB  
Article
The Genetic Elements of the Obesity Paradox in Atherosclerosis Identified in an Intercross Between Hyperlipidemic Mouse Strains
by Mei-Hua Chen, Bilhan Chagari, Ashley M. Abramson, Lisa J. Shi, Jiang He and Weibin Shi
Int. J. Mol. Sci. 2025, 26(9), 4241; https://doi.org/10.3390/ijms26094241 - 29 Apr 2025
Abstract
Overweight and obese individuals show lower mortality rates or better prognoses than those of normal weight in a variety of diseases, a phenomenon called the “obesity paradox”. An inverse association of adiposity with atherosclerosis has been observed in both humans and mice. To [...] Read more.
Overweight and obese individuals show lower mortality rates or better prognoses than those of normal weight in a variety of diseases, a phenomenon called the “obesity paradox”. An inverse association of adiposity with atherosclerosis has been observed in both humans and mice. To dissect phenotypic and genetic connections between the traits, 154 female and 145 male F2 mice were generated from an intercross between BALB/cJ and LP/J apolipoprotein E-deficient mice and fed a Western diet for 12 weeks. Atherosclerotic lesion size in the aortic root, body weight, plasma lipids, and glucose were measured, and genotyping was performed on miniMUGA SNP arrays. Quantitative trait locus (QTL) analyses on all F2 mice with sex as a covariate revealed four significant QTLs on chromosomes (Chr) 3, 6, 13, and 15 for atherosclerosis and three significant QTLs on Chr2, 7, and 15 for body weight. Chr15 QTL for atherosclerosis overlapped with one for body weight near 36 Mb. After adjusting for variation in body weight, Chr15 atherosclerosis QTL was downgraded from significant to suggestive linkage. Body weight was inversely correlated with atherosclerotic lesion sizes and accounted for more variance than a single other risk factor for atherosclerosis among F2 mice. Analysis of public data collected from two backcross cohorts revealed strong correlations between body weight and fat mass in adult mice (r ≥ 0.93; p ≤ 1.6 × 10−136). Thus, the obesity paradox in atherosclerosis is partially attributable to shared genetic components that have an opposite effect on adiposity and atherosclerosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms Linking Obesity to Atherosclerosis Pathogenesis)
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