Inflammation: The Major Player in Metabolic Syndrome

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 1732

Special Issue Editor


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Guest Editor
1. Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA
2. Division of Endocrinology, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA 15224, USA
Interests: glucose and lipid metabolism and metabolic disorders; inflammasomes; energy metabolism; glucose homeostasis
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Special Issue Information

Dear Colleagues,

Metabolic disorders, including obesity, type 2 diabetes mellitus (T2DM), cardiovascular diseases, and fatty liver disease, are leading causes for preventable death in the U.S. and worldwide, and are a huge healthcare burden in terms of economics, quality of life, and morbidity/mortality. Inflammation has become one of the hottest research areas in the field of metabolic disorders in recent years.  Inflammasomes are part of the innate immune system. They are intracellular oligomers that act as receptors and sensors that regulate the production of interleukin (IL)-1β and IL-18 in response to infectious microbes or molecules.

Recent research has demonstrated that inflammasomes are also involved in the regulation of energy metabolism and whole-body glucose homeostasis, indicating that inflammasomal proteins could be novel targets for treating metabolic disorders. Thus, this Special Issue aims to highlight recent advances in our understanding of the role of inflammasomes in energy metabolism, glucose homeostasis, and underlying molecular mechanisms. We invite you to submit your original research articles as well as review articles to facilitate the understanding of this newer field.

Dr. Zhenwei Gong
Guest Editor

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Keywords

  • inflammasomes
  • energy metaboism
  • metabolic syndrome
  • chronic inflammation
  • cytokine production

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Published Papers (1 paper)

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Research

16 pages, 5816 KiB  
Article
Single-Cell RNA Sequencing Reveals Macrophage Dynamics During MASH in Leptin-Deficient Rats
by Xiaoming Xin, Yaohua Ni, Jing Wang, Fenglin Wu, Meichen Liu, Lingjuan Wu, Jiaxing Dai, Chenglin Wu, Xiaolei Song, Wang Zhang, Guangrui Yang, Ruling Shen and Xianmin Zhu
Cells 2025, 14(2), 96; https://doi.org/10.3390/cells14020096 - 10 Jan 2025
Viewed by 1274
Abstract
Macrophages play important roles in metabolic dysfunction-associated steatohepatitis (MASH), an advanced and inflammatory stage of metabolic dysfunction-associated steatotic liver disease (MASLD). In humans and mice, the cellular heterogeneity and diverse function of hepatic macrophages in MASH have been investigated by single cell RNA [...] Read more.
Macrophages play important roles in metabolic dysfunction-associated steatohepatitis (MASH), an advanced and inflammatory stage of metabolic dysfunction-associated steatotic liver disease (MASLD). In humans and mice, the cellular heterogeneity and diverse function of hepatic macrophages in MASH have been investigated by single cell RNA sequencing (scRNA-seq). However, little is known about their roles in rats. Here, we collected liver tissues at the postnatal week 16, when our previously characterized Lep∆I14/∆I14 rats developed MASH phenotypes. By scRNA-seq, we found an increase in the number of macrophages and endothelial cells and a decrease in that of NK and B cells. Hepatic macrophages in rats underwent a unique M1 to M2 transition without expression of the classical markers such as Arg1 and Nos2, except for Cd163. Lipid-associated macrophages (LAMs) were increased, which could be detected by the antibody against Cd63. In the microenvironment, macrophages had an increased number of interactions with hepatocytes, myofibroblasts, T cells, neutrophils, and dendritic cells, while their interaction strengths remained unchanged. Finally, the macrophage migration inhibitory factor (MIF) pathway was identified as the top upregulated cell-communication pathway in MASH. In conclusion, we dissected hepatic macrophage dynamics during MASH at single cell resolution and provided fundamental tools for the investigation of MASH in rat models. Full article
(This article belongs to the Special Issue Inflammation: The Major Player in Metabolic Syndrome)
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