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      How inflammation dictates diabetic peripheral neuropathy: An enlightening review

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          Abstract

          Background

          Diabetic peripheral neuropathy (DPN) constitutes a debilitating complication associated with diabetes. Although, the past decade has seen rapid developments in understanding the complex etiology of DPN, there are no approved therapies that can halt the development of DPN, or target the damaged nerve. Therefore, clarifying the pathogenesis of DPN and finding effective treatment are the crucial issues for the clinical management of DPN.

          Aims

          This review is aiming to summary the current knowledge on the pathogenesis of DPN, especially the mechanism and application of inflammatory response.

          Methods

          We systematically summarized the latest studies on the pathogenesis and therapeutic strategies of diabetic neuropathy in PubMed.

          Results

          In this seminal review, the underappreciated role of immune activation in the progression of DPN is scrutinized. Novel insights into the inflammatory regulatory mechanisms of DPN have been unearthed, illuminating potential therapeutic strategies of notable clinical significance. Additionally, a nuanced examination of DPN's complex etiology, including aberrations in glycemic control and insulin signaling pathways, is presented. Crucially, an emphasis has been placed on translating these novel understandings into tangible clinical interventions to ameliorate patient outcomes.

          Conclusions

          This review is distinguished by synthesizing cutting‐edge mechanisms linking inflammation to DPN and identifying innovative, inflammation‐targeted therapeutic approaches.

          Abstract

          Understanding the role of inflammation in diabetic peripheral neuropathy's progression.

          Related collections

          Most cited references176

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          Origin and physiological roles of inflammation.

          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)

            (1998)
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              Biochemistry and molecular cell biology of diabetic complications.

              Diabetes-specific microvascular disease is a leading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke and limb amputation. Four main molecular mechanisms have been implicated in glucose-mediated vascular damage. All seem to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain. This integrating paradigm provides a new conceptual framework for future research and drug discovery.
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                Author and article information

                Contributors
                dbinbin@aliyun.com
                Journal
                CNS Neurosci Ther
                CNS Neurosci Ther
                10.1111/(ISSN)1755-5949
                CNS
                CNS Neuroscience & Therapeutics
                John Wiley and Sons Inc. (Hoboken )
                1755-5930
                1755-5949
                05 October 2023
                April 2024
                : 30
                : 4 ( doiID: 10.1002/cns.v30.4 )
                : e14477
                Affiliations
                [ 1 ] Center for Rehabilitation Medicine, Department of Neurology, Zhejiang Provincial People's Hospital Affiliated People's Hospital, Hangzhou Medical College Hangzhou China
                [ 2 ] Department of Neurology First Affiliated Hospital of Wenzhou Medical University Wenzhou Zhejiang Province China
                [ 3 ] First School of Clinical Medicine Wenzhou Medical University Wenzhou Zhejiang Province China
                [ 4 ] Department of Neurology, Shanghai East Hospital Tongji University Shanghai P.R. China
                [ 5 ] Department of Geriatrics The Affiliated Hospital of Qingdao University Qingdao Shandong Province China
                [ 6 ] Department of Pediatrics Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Wenzhou China
                Author notes
                [*] [* ] Correspondence

                Binbin Deng, Department of Neurology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.

                Email: dbinbin@ 123456aliyun.com

                Author information
                https://orcid.org/0000-0002-4058-0738
                Article
                CNS14477 CNSNT-2023-1018.R1
                10.1111/cns.14477
                11017439
                37795833
                5d2c305b-704a-4f36-8c6f-463e528324b8
                © 2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 August 2023
                : 17 July 2023
                : 08 September 2023
                Page count
                Figures: 5, Tables: 2, Pages: 15, Words: 9554
                Funding
                Funded by: Medical Science and Technology Project of Zhejiang Province , doi 10.13039/501100017594;
                Award ID: 2022KY506
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 81901273
                Funded by: Science Technology Department of Zhejiang Province
                Award ID: Q21H090076
                Categories
                Review
                Reviews
                Custom metadata
                2.0
                April 2024
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.4.0 mode:remove_FC converted:15.04.2024

                Neurosciences
                diabetic neuropathy,inflammatory response,metabolic changes,molecular mechanism
                Neurosciences
                diabetic neuropathy, inflammatory response, metabolic changes, molecular mechanism

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