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Molecular Mechanisms in Diabetic Neuropathy
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Molecular Mechanisms in Diabetic Neuropathy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 2399

Special Issue Editor

Prof. Dr. Yun Gao

E-Mail Website
Guest Editor
Department of Physiology, The Basic Medical College of Nanchang University, Nanchang 330006, China
Interests: chronic pain; diabetic neuropathic pain; major depressive disorder; purinergic signalling

Special Issue Information

Dear Colleagues,

Diabetes is a metabolic disease characterized by high blood glucose levels, which are caused by a complex combination of genetic factors and environmental factors. Epidemiological studies have shown that with continuous improvements in people's living standards, an aging population, and lifestyle changes, diabetes prevalence has rapidly grown year by year. Diabetic patients often suffer from complications, for example, cardiovascular disease, retinopathy, and neuropathy. Diabetic neuropathy is a common diabetic complication, which seriously affects the life quality of patients.

Although diabetic neuropathy is one of the main symptoms of diabetic complications, its pathophysiological mechanisms are not yet fully understood and need further research. The objective of this Special Issue is to collect original and review articles to provide the most updated molecular knowledge in the field of diabetic neuropathy.

Suggested topics include, but are not limited to, studies and updated reviews on the molecular mechanisms of diabetic neuropathy in in vivo or in vitro clinic or animal experiments.

Prof. Dr. Yun Gao
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

  • diabetic neuropathy
  • diabetic neuropathic pain
  • diabetes mellitus

Published Papers (2 papers)

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Research

18 pages, 3670 KiB  
Article
Implication of lncRNA MSTRG.81401 in Hippocampal Pyroptosis Induced by P2X7 Receptor in Type 2 Diabetic Rats with Neuropathic Pain Combined with Depression
by Ting Zhan, Shanshan Tang, Junpei Du, Jingshuang Liu, Bodong Yu, Yuxin Yang, Yuting Xie, Yanting Qiu, Guodong Li and Yun Gao
Int. J. Mol. Sci. 2024, 25(2), 1186; https://doi.org/10.3390/ijms25021186 - 18 Jan 2024
Cited by 1 | Viewed by 1073
Abstract
Major depressive disorder (MDD) is a common complication of diabetes and is often observed alongside diabetic neuropathic pain (DNP) as a comorbidity in diabetic patients. Long non-coding RNA (lncRNA) plays an important role in various pathophysiological processes. The P2X7 receptor is responsible for [...] Read more.
Major depressive disorder (MDD) is a common complication of diabetes and is often observed alongside diabetic neuropathic pain (DNP) as a comorbidity in diabetic patients. Long non-coding RNA (lncRNA) plays an important role in various pathophysiological processes. The P2X7 receptor is responsible for triggering inflammatory responses, such as pyroptosis, linked to pain and depression. The aim of this study was to investigate the effect of lncRNA MSTRG.81401 on hippocampal pyroptosis induced by the P2X7 receptor in diabetic rats with DNP combined with MDD (DNP + MDD). Our results showed that the expression of lncRNA MSTRG.81401 was significantly elevated in the hippocampus of DNP + MDD rats compared with the control group. Following the administration of shRNA targeting lncRNA MSTRG.81401, a notable elevation in mechanical and thermal pain thresholds was observed in rats with comorbid DNP and MDD. Additionally, significant improvements in depression-like behaviors were evident in the open-field test (OFT), sucrose preference test (SPT), and forced swim test (FST). In the DNP + MDD rats, elevated levels in hippocampal P2X7 receptor mRNA and protein were observed, along with increased co-expression of P2X7 and the astrocytic marker glial fibrillary acidic protein (GFAP). Meanwhile, in DNP + MDD rats, the heightened mRNA expression of NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), pyroptosis-related protein Gasdermin D (GSDMD), caspase-1, IL-1β, IL-18, and TNF-α was detected, in addition to increased serum levels of IL-1β, IL-18 and TNF-α. After shRNA treatment with lncRNA MSTRG.81401, the above abnormal changes in indicators for pyroptosis and inflammation were improved. Therefore, our study demonstrates that shRNA of lncRNA MSTRG.81401 can alleviate the pain and depression-like behaviors in diabetic rats associated with the comorbidity of DNP and MDD by inhibiting the hippocampal P2X7 receptor-mediated pyroptosis pathway and pro-inflammatory responses. This suggests that the P2X7R/NLRP3/caspase-1 implicated pyroptosis and inflammatory scenario may serve as a potential target for the management of comorbid DNP and MDD in diabetes. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Diabetic Neuropathy)
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25 pages, 5332 KiB  
Article
Neuroprotective Effects of a Hydrogen Sulfide Donor in Streptozotocin-Induced Diabetic Rats
by Abdulaziz M. F. Shayea, Waleed M. Renno, Bedoor Qabazard and Willias Masocha
Int. J. Mol. Sci. 2023, 24(23), 16650; https://doi.org/10.3390/ijms242316650 - 23 Nov 2023
Cited by 1 | Viewed by 857
Abstract
Diabetic neuropathy is an important long-term complication of diabetes. This study explored the hypothesis that hydrogen sulfide (H2S) ameliorates neuropathic pain by controlling antiapoptotic and pro-apoptotic processes. The effects of a slow-releasing H2S donor, GYY4137, on the expression of [...] Read more.
Diabetic neuropathy is an important long-term complication of diabetes. This study explored the hypothesis that hydrogen sulfide (H2S) ameliorates neuropathic pain by controlling antiapoptotic and pro-apoptotic processes. The effects of a slow-releasing H2S donor, GYY4137, on the expression of antiapoptotic and pro-apoptotic genes and proteins, such as B-cell lymphoma 2 (Bcl2) and Bcl-2-like protein 4 (Bax), as well as caspases, cyclooxygenase (COX)-1 and COX-2, monocytes/macrophages, and endothelial cells, in the spinal cord of male Sprague-Dawley rats with streptozotocin-induced peripheral diabetic neuropathy, were investigated using reverse transcription-PCR, western blot and immunohistochemistry. The antihypoalgesic activities of GYY4137 on diabetic rats were evaluated using the tail flick test. Treatment of diabetic rats with GYY4137 attenuated thermal hypoalgesia and prevented both the diabetes-induced increase in Bax mRNA expression (p = 0.0032) and the diabetes-induced decrease in Bcl2 mRNA expression (p = 0.028). The GYY4137-treated diabetic group had increased COX-1 (p = 0.015), decreased COX-2 (p = 0.002), reduced caspase-7 and caspase-9 protein expression (p < 0.05), and lower numbers of endothelial and monocyte/macrophage cells (p < 0.05) compared to the non-treated diabetic group. In summary, the current study demonstrated the protective properties of H2S, which prevented the development of neuropathy related behavior, and suppressed apoptosis activation pathways and inflammation in the spinal cord. H2S-releasing drugs could be considered as possible treatment options of diabetic peripheral neuropathy. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Diabetic Neuropathy)
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