- 1The First Affiliated Hospital, Department of Metabolism and Endocrinology, Hengyang Medical School, University of South China, Hengyang, Hunan, China
- 2The First Affiliated Hospital, Department of Clinical Laboratory Medicine, Institution of Microbiology and Infectious Diseases, Hengyang Medical School, University of South China, Hengyang, Hunan, China
- 3Department of Pathology and Laboratory Medicine, Kaiser Permanente Sacramento Medical Center, Sacramento, CA, United States
Editorial on the Research Topic
The role of exosomes and organokines in metabolic and endocrine disease
The field of exosomes and organokines biology and metabolism is rapidly expanding. Increasing numbers of exosomal miRNA have also been used as biomarkers for metabolic diseases in clinical settings, such as miR-34a,miR-122,miR-192,miR-142, and so on (1–4). Several biological factors including miR-130a-3p and miR-3075 are packaged into exosomes and then transported into specific organs to regulate local metabolism (5–7). Novel-identified organokines (adipokines, myokines, hepatokines) have been reported to play crucial roles in the regulation of whole-body metabolism homeostasis (8–10) affecting the regulation of glucose metabolism, lipid metabolism, insulin sensitivity, oxidative stress, low-grade inflammation and so on. The goal of this Research Topic “The Role of Exosomes and Organokines in Metabolic and Endocrine Disease” is to highlight a wide range of exosomes and organokines originating from the metabolic organs that mediate inter-organ crosstalk and participate in the development of metabolic diseases. Six high-quality papers (Pang et al., Chen et al., Sun et al., Mei et al., Wang et al., 11) were accepted by the Frontiers editorial team for publication in the Frontiers in Endocrinology. They provide new information to the advancement of organokines and exosome-based diagnostics and therapeutic approaches for metabolic and endocrine diseases.
In this Research Topic, Pang et al. first described the expression profile of plasma exosomal long non-coding RNAs (lncRNAs) in patients with type 1 diabetes mellitus (T1DM). That study demonstrated that 162 aberrantly expressed exosomal lncRNAs including 77 up-regulated and 85 down-regulated were associated with the pathogenesis of T1DM. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed and indicated that these differentially expressed lncRNAs were involved in oxidative phosphorylation. This work provided a novel insight into the pathogenesis of T1DM and a foundation for using exosomal lncRNAs as potential diagnostic biomarkers and therapeutic targets for T1DM.
In the field of diabetic vascular complications (DVC), Chen et al. summarized the most recently published research suggesting the changes in the production process of exosomes in the diabetic microenvironment and the early warning role of exosomes in DVC from different systems and their pathological processes. Additionally, mechanisms of various stem cells through exosomes for the treatment of DVC were also discussed. For example, stem cells can secrete a variety of factors through the exosome pathway to promote the formation of new blood vessels. Furthermore, bone marrow mesenchymal stem cell-derived exosomes could inhibit the mTOR signaling pathway to enhance autophagy, which has a protective effect on kidney injury induced by hyperglycemia. In another article, Sun et al. described the multiple roles of exosomes in the pathology and treatment of diabetes and diabetic complications and emphasized that the pathological molecular spectrum formed by miRNAs and microproteins carried by exosomes from the body fluids of diabetic patients may provide possible new therapeutic ideas for DVC in the future.
Regarding the critical role of adipose tissue-derived exosomes in metabolic diseases such as destroying epithelial cells, disrupting blood vessels, aggravating liver fibrosis, and promoting the transformation of monocyte to both macrophage (M1 pro-inflammatory phenotype) and macrophage (M2 anti-inflammatory phenotype). Mei et al. reviewed recent advances in the role of adipose tissue-derived exosomes in metabolic diseases. In addition, current barriers hindering exosome-based therapeutic strategies are discussed.
Wang et al. discussed how organokines (adipokines, gut microbiota and their metabolites, intestinal cytokines, myokines, and hepatokines) and exosomes (adipocytes, skeletal muscle, and hepatocyte-derived exosomes) act as important triggers for adipose tissue macrophage recruitment and adipose tissue macrophage polarization, providing further insight into obesity treatment. In addition, they highlighted the complex interactions between various organokines and exosomes in the obese state, further revealing new pathways for the recruitment and polarization of adipose tissue macrophages.
The liver plays a vital role in modulating energy homeostasis. In modulating systemic glucolipid metabolism, most of the attributions for the release of hepatokines that maintain metabolic homeostasis in autocrine, endocrine and paracrine pathways that govern connections between the liver and other organs. Chen et al. (11) highlighted the interaction of some feeding-induced hepatokines such as Adropin, MANF, Leap2 and PCSK9 in the liver and extrahepatic tissues such as brain, adipose, heart, and pancreatic tissues, and also clarified the potential mechanisms by which these hepatokines mediate crosstalk between the liver and other organs. Targeting these feeding-induced hepatokines is expected to be a possible therapeutic approach for T2DM to help in control and treatment.
In conclusion, exosomes and organokines exert immunomodulatory functions through a variety of novel mechanisms that are valuable for the prediction and treatment of diabetes and its complications, obesity, and some metabolic diseases. The original research articles and review articles included in this issue present a range of topics that are under active investigation. With extensive investigations, additional pathological/beneficial roles of exosomes and organokines in diabetes and its complications and metabolic diseases are revealed to improve our understanding of exosomes and organokines and to elucidate the development of exosomal and organokines-based therapeutic strategies for more accurate diagnosis and more effective treatment of metabolic diseases. However, despite the recognition of the importance of exosomes and organokines in metabolic diseases, the specific regulatory mechanisms of these diseases are not fully understood and should remain a key focus of future research.
Author contributions
X-HX, Q-YW, JL and Z-ZL conceived and wrote the manuscript. All authors contributed to the article and approved the submitted version.
Funding
This systematic received funding from the National Natural Science Foundation of China (82070873, 82000813), the Natural Science Foundation of Hunan province (2020JJ8097, 2021JJ40496, 2020SK51814), and major special projects of Hunan Provincial Health and Family Planning Commission (A2017011).
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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Keywords: organokines, obesity, diabetes, metabolic syndrome, endocrine diseases, exosomes
Citation: Wang Q-Y, Liao Z-Z, Lai J and Xiao X-H (2023) Editorial: The role of exosomes and organokines in metabolic and endocrine disease. Front. Endocrinol. 14:1198791. doi: 10.3389/fendo.2023.1198791
Received: 02 April 2023; Accepted: 17 April 2023;
Published: 21 April 2023.
Edited and Reviewed by:
Ralf Jockers, Université Paris Cité, FranceCopyright © 2023 Wang, Liao, Lai and Xiao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Xin-Hua Xiao, xinhua0102@163.com; Jinping Lai, jinping.x.lai@kp.org
†These authors have contributed equally to this work