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Biology
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Pathogenic Factors and Key Pathways of Metabolic Diseases
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Pathogenic Factors and Key Pathways of Metabolic Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 5813

Special Issue Editor

Dr. Aijun Qiao

E-Mail Website1 Website2
Guest Editor
1. School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
2. ZhongShan Institute for Drug Discovery, Chinese Academy of Sciences, Guangzhou 528400, China
Interests: metabolism diseases; lipid overload; insulin resistance; pathogenic molecules; biomarkers; drug therapy

Special Issue Information

Dear Colleagues,

The increasing incidence of metabolic diseases, such as type 2 diabetes mellitus (T2DM), hyperlipidemia (HLD), nonalcoholic fatty liver disease (NAFLD) and obesity, poses a great burden on global health. Many of them may occur at the same time and share common risk factors, which makes diagnosis and treatments more difficult. Although progress has been made in the pathogenesis of metabolic diseases, there is a need to continue exploring related pathogenic factors and key pathways to develop new diagnostic and drug targets. We are pleased to invite you to our Special Issue, entitled “Pathogenic Factors and Key Pathways of Metabolic Diseases”. The aim of this Special Issue is to report the most recent advances in the field of pathogenic pathways in metabolic diseases. We seek new studies focusing on the mechanisms of metabolic diseases, as well as on the common pathogenic factors and new applications of diseases diagnosis. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Key pathogenic pathways of metabolic diseases;
  • New biomarkers or drug targets of metabolic diseases;
  • Common pathogenic molecules in different metabolic diseases.

Dr. Aijun Qiao
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. Biology 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

  • metabolism diseases
  • lipid overload
  • insulin resistance
  • pathogenic molecules
  • biomarkers
  • drug therapy

Published Papers (3 papers)

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Review

29 pages, 3267 KiB  
Review
Glycolipid Metabolic Disorders, Metainflammation, Oxidative Stress, and Cardiovascular Diseases: Unraveling Pathways
by Enzo Pereira de Lima, Renato Cesar Moretti, Jr., Karina Torres Pomini, Lucas Fornari Laurindo, Kátia Portero Sloan, Lance Alan Sloan, Marcela Vialogo Marques de Castro, Edgar Baldi, Jr., Bruna Fidencio Rahal Ferraz, Eliana de Souza Bastos Mazuqueli Pereira, Virgínia Maria Cavallari Strozze Catharin, Carolina Haber Mellen, Flávia Cristina Castilho Caracio, Caio Sérgio Galina Spilla, Jesselina F. S. Haber and Sandra Maria Barbalho
Biology 2024, 13(7), 519; https://doi.org/10.3390/biology13070519 - 12 Jul 2024
Viewed by 285
Abstract
Glycolipid metabolic disorders (GLMDs) are various metabolic disorders resulting from dysregulation in glycolipid levels, consequently leading to an increased risk of obesity, diabetes, liver dysfunction, neuromuscular complications, and cardiorenal vascular diseases (CRVDs). In patients with GLMDs, excess caloric intake and a lack of [...] Read more.
Glycolipid metabolic disorders (GLMDs) are various metabolic disorders resulting from dysregulation in glycolipid levels, consequently leading to an increased risk of obesity, diabetes, liver dysfunction, neuromuscular complications, and cardiorenal vascular diseases (CRVDs). In patients with GLMDs, excess caloric intake and a lack of physical activity may contribute to oxidative stress (OxS) and systemic inflammation. This study aimed to review the connection between GLMD, OxS, metainflammation, and the onset of CRVD. GLMD is due to various metabolic disorders causing dysfunction in the synthesis, breakdown, and absorption of glucose and lipids in the body, resulting in excessive ectopic accumulation of these molecules. This is mainly due to neuroendocrine dysregulation, insulin resistance, OxS, and metainflammation. In GLMD, many inflammatory markers and defense cells play a vital role in related tissues and organs, such as blood vessels, pancreatic islets, the liver, muscle, the kidneys, and adipocytes, promoting inflammatory lesions that affect various interconnected organs through their signaling pathways. Advanced glycation end products, ATP-binding cassette transporter 1, Glucagon-like peptide-1, Toll-like receptor-4, and sphingosine-1-phosphate (S1P) play a crucial role in GLMD since they are related to glucolipid metabolism. The consequences of this is system organ damage and increased morbidity and mortality. Full article
(This article belongs to the Special Issue Pathogenic Factors and Key Pathways of Metabolic Diseases)
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26 pages, 1432 KiB  
Review
Intestinal Barrier Dysfunction and Gut Microbiota in Non-Alcoholic Fatty Liver Disease: Assessment, Mechanisms, and Therapeutic Considerations
by Changrui Long, Xiaoyan Zhou, Fan Xia and Benjie Zhou
Biology 2024, 13(4), 243; https://doi.org/10.3390/biology13040243 - 6 Apr 2024
Viewed by 2366
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a type of metabolic stress liver injury closely related to insulin resistance (IR) and genetic susceptibility without alcohol consumption, which encompasses a spectrum of liver disorders ranging from simple hepatic lipid accumulation, known as steatosis, to the [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is a type of metabolic stress liver injury closely related to insulin resistance (IR) and genetic susceptibility without alcohol consumption, which encompasses a spectrum of liver disorders ranging from simple hepatic lipid accumulation, known as steatosis, to the more severe form of steatohepatitis (NASH). NASH can progress to cirrhosis and hepatocellular carcinoma (HCC), posing significant health risks. As a multisystem disease, NAFLD is closely associated with systemic insulin resistance, central obesity, and metabolic disorders, which contribute to its pathogenesis and the development of extrahepatic complications, such as cardiovascular disease (CVD), type 2 diabetes mellitus, chronic kidney disease, and certain extrahepatic cancers. Recent evidence highlights the indispensable roles of intestinal barrier dysfunction and gut microbiota in the onset and progression of NAFLD/NASH. This review provides a comprehensive insight into the role of intestinal barrier dysfunction and gut microbiota in NAFLD, including intestinal barrier function and assessment, inflammatory factors, TLR4 signaling, and the gut–liver axis. Finally, we conclude with a discussion on the potential therapeutic strategies targeting gut permeability and gut microbiota in individuals with NAFLD/NASH, such as interventions with medications/probiotics, fecal transplantation (FMT), and modifications in lifestyle, including exercise and diet. Full article
(This article belongs to the Special Issue Pathogenic Factors and Key Pathways of Metabolic Diseases)
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14 pages, 1854 KiB  
Review
Exosomes: New Insights into the Pathogenesis of Metabolic Syndrome
by Ning Wang, Jing Li, Zixuan Hu, Ebenezeri Erasto Ngowi, Baolong Yan and Aijun Qiao
Biology 2023, 12(12), 1480; https://doi.org/10.3390/biology12121480 - 1 Dec 2023
Viewed by 2523
Abstract
Exosomes are a subtype of extracellular vesicles (EVs) with a diameter of 30~150 nm (averaging ~100 nm) that are primarily produced through the endosomal pathway, and carry various components such as lipids, proteins, RNA, and other small molecular substances. Exosomes can mediate intercellular [...] Read more.
Exosomes are a subtype of extracellular vesicles (EVs) with a diameter of 30~150 nm (averaging ~100 nm) that are primarily produced through the endosomal pathway, and carry various components such as lipids, proteins, RNA, and other small molecular substances. Exosomes can mediate intercellular communication through the bioactive substances they carry, thus participating in different physiological activities. Metabolic syndrome (MS) is a disease caused by disturbances in the body’s metabolism, mainly including insulin resistance (IR), diabetes, obesity, non-alcoholic fatty liver disease (NAFLD), hyperlipidemia, and atherosclerosis (AS). Recent studies have shown that exosomes are closely related to the occurrence and development of MS. Exosomes can act as messengers to mediate signaling transductions between metabolic cells in the organism and play a bidirectional regulatory role in the MS process. This paper mainly reviews the components, biogenesis, biological functions and potential applications of exosomes, and exosomes involved in the pathogenesis of MS as well as their clinical significance in MS diagnosis. Full article
(This article belongs to the Special Issue Pathogenic Factors and Key Pathways of Metabolic Diseases)
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