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Biomedicines
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Metabolic Disorders and Their Complications: From Molecular Mechanisms to Therapeutic...
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Metabolic Disorders and Their Complications: From Molecular Mechanisms to Therapeutic Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1887

Special Issue Editors

Dr. Sandeep Kumar

E-Mail Website
Guest Editor
Department of Microbiology/ Immunology, Tulane University, New Orleans, LA 70112, USA
Interests: diabetes; obesity; inflammatory disease; necroptosis; sarcopenia
Special Issues, Collections and Topics in MDPI journals
Dr. Abhishek Gupta

E-Mail Website
Guest Editor
Department of Biochemistry and Structural Biology, Joe R. & Teresa Lozano Long School of Medicine, University of Texas Health Science center, San Antonio, TX, USA
Interests: metabolic disease; lipid metabolism; type 2 diabetes; obesity
Special Issues, Collections and Topics in MDPI journals
Dr. Atul Kumar Pandey

E-Mail Website
Co-Guest Editor
Department of Entomology, University of Kentucky, Lexington, KY, USA
Interests: sleep physiology and immunobiology; nanoparticles; medicinal plants

Special Issue Information

Dear Colleagues,

Metabolic disturbances refer to disruptions in the body's normal chemical processes, specifically those involved in converting food into energy and utilizing nutrients, which are responsible for various functions such as breathing, circulation, and growth. These disturbances can cause metabolic disorders, which are mainly associated with nutrients, energy, and other essential molecules. The main causes of these problems are linked to biochemical pathways that regulate metabolism, due to genetic defects, lifestyle factors, or a combination of both. They can impact various organs and systems in the body, leading to a wide range of complications. The prevalence of metabolic disorders is increasing rapidly worldwide. The key signaling pathways that regulate metabolism include insulin signaling, AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), and other critical metabolic regulators. Metabolic disease is also influenced by the effects of environmental factors, such as diet and lifestyle, on the expression of genes related to metabolic regulation and disease susceptibility. Therefore, we must take control of these metabolic problems in order to improve human health. The main metabolism-related disorders are as follows:

  • Diabetes;
  • Obesity and metabolic syndrome;
  • Polycystic ovarian syndrome;
  • Cardiovascular disease;
  • Neurological complications;
  • Kidney problems;
  • Endocrine dysfunction;
  • Cancer risk.

Dr. Sandeep Kumar
Dr. Abhishek Gupta
Dr. Atul Kumar Pandey
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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. Biomedicines 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 2600 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

  • metabolism
  • diabetes
  • obesity
  • nutrition
  • AMPK and mTOR

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Published Papers (1 paper)

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Research

16 pages, 3381 KB  
Article
Multi-Omics Evidence Linking Depression to MASLD Risk via Inflammatory Immune Signaling
by Keye Lin, Yiwei Liu, Xitong Liang, Yiming Zhang, Zijie Luo, Fei Chen, Runhua Zhang, Peiyu Ma and Xiang Chen
Biomedicines 2026, 14(1), 174; https://doi.org/10.3390/biomedicines14010174 - 13 Jan 2026
Viewed by 1180
Abstract
Background: Depression and Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD) are common chronic diseases, respectively. However, the causal and molecular links between them remain unclear. In order to explore whether depression contributes to an increased risk of MASLD and whether inflammation mediates [...] Read more.
Background: Depression and Metabolic Dysfunction-Associated Steatotic Fatty Liver Disease (MASLD) are common chronic diseases, respectively. However, the causal and molecular links between them remain unclear. In order to explore whether depression contributes to an increased risk of MASLD and whether inflammation mediates this effect, we integrated multi-level evidence from the epidemiology of the National Health and Nutrition Examination Survey (NHANES), the genetics of GWAS, the transcriptomes of GEO, and single-cell RNA sequencing datasets. Methods: A multi-level integrative analysis strategy was used to validate this pathway. First, a cross-sectional epidemiological analysis based on NHANES data was used to reveal the association between depression and MASLD, and to explore the mediating role of inflammation and liver injury markers. Secondly, a two-sample Mendelian randomization analysis was used to infer the causal direction of depression and MASLD, and to verify the mediating effect of systemic inflammation and liver injury indicators at the genetic level. Then, the transcriptome co-expression network analysis and machine learning were used to screen the common hub genes connecting the two diseases. Finally, single-cell transcriptome data were used to characterize the dynamic expression of potential key genes during disease progression at cellular resolution. Results: Depression significantly increased the risk of MASLD, especially in women (OR = 1.39, 95%CI [1.17–1.65]). Parallel mediation analysis showed that high-sensitivity C-reactive protein (hs-CRP) (p < 0.001), γ-glutamyltransferase (GGT) (p < 0.001), and alkaline phosphatase (ALP) (p < 0.001) mediated this relationship. Mendelian randomization analysis confirmed the unidirectional causal effect of depression on MASLD, and there was no reverse association (β = 0.483, SE = 0.146, p = 0.001). Weighted gene co-expression network analysis and machine learning identified CD40LG as a potential molecular bridge between depression-associated immune modules and MASLD. In addition, single-cell data analysis revealed a stage-specific trend of CD40LG expression in CD4+ T cells during MASLD progression, while its receptor CD40 was also activated in B cells. In the female sample, CD40LG maintained an upward trend. However, the stability of this result is limited by the limited sample size. Conclusions: This study provides converging multi-omics evidence that depression plays a causal role in MASLD through inflammation-mediated immune signaling. The CD40LG-CD40 axis has emerged as an immune mechanism that transposes depression into the pathogenesis of MASLD, providing a potential target for the intervention of gender-specific metabolic liver disease. Full article
(This article belongs to the Special Issue Metabolic Disorders and Their Complications: From Molecular Mechanisms to Therapeutic Perspectives)
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