Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment
Diabetic peripheral neuropathy (DPN) refers to the development of peripheral nerve dysfunction in patients with diabetes when other causes are excluded. Diabetic distal symmetric polyneuropathy (DSPN) is the most representative form of DPN. As one of the most common complications of diabetes, its pr...
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| Format: | Article |
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Frontiers Media S.A.
2024-01-01
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| Series: | Frontiers in Endocrinology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2023.1265372/full |
| _version_ | 1797361000654045184 |
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| author | Jinxi Zhu Jinxi Zhu Ziyan Hu Ziyan Hu Yifan Luo Yinuo Liu Wei Luo Xiaohong Du Zhenzhong Luo Jialing Hu Shengliang Peng |
| author_facet | Jinxi Zhu Jinxi Zhu Ziyan Hu Ziyan Hu Yifan Luo Yinuo Liu Wei Luo Xiaohong Du Zhenzhong Luo Jialing Hu Shengliang Peng |
| author_sort | Jinxi Zhu |
| collection | DOAJ |
| description | Diabetic peripheral neuropathy (DPN) refers to the development of peripheral nerve dysfunction in patients with diabetes when other causes are excluded. Diabetic distal symmetric polyneuropathy (DSPN) is the most representative form of DPN. As one of the most common complications of diabetes, its prevalence increases with the duration of diabetes. 10-15% of newly diagnosed T2DM patients have DSPN, and the prevalence can exceed 50% in patients with diabetes for more than 10 years. Bilateral limb pain, numbness, and paresthesia are the most common clinical manifestations in patients with DPN, and in severe cases, foot ulcers can occur, even leading to amputation. The etiology and pathogenesis of diabetic neuropathy are not yet completely clarified, but hyperglycemia, disorders of lipid metabolism, and abnormalities in insulin signaling pathways are currently considered to be the initiating factors for a range of pathophysiological changes in DPN. In the presence of abnormal metabolic factors, the normal structure and function of the entire peripheral nervous system are disrupted, including myelinated and unmyelinated nerve axons, perikaryon, neurovascular, and glial cells. In addition, abnormalities in the insulin signaling pathway will inhibit neural axon repair and promote apoptosis of damaged cells. Here, we will discuss recent advances in the study of DPN mechanisms, including oxidative stress pathways, mechanisms of microvascular damage, mechanisms of damage to insulin receptor signaling pathways, and other potential mechanisms associated with neuroinflammation, mitochondrial dysfunction, and cellular oxidative damage. Identifying the contributions from each pathway to neuropathy and the associations between them may help us to further explore more targeted screening and treatment interventions. |
| first_indexed | 2024-03-08T15:47:41Z |
| format | Article |
| id | doaj.art-553aafa46e464fc193843423bc157369 |
| institution | Directory Open Access Journal |
| issn | 1664-2392 |
| language | English |
| last_indexed | 2024-03-08T15:47:41Z |
| publishDate | 2024-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj.art-553aafa46e464fc193843423bc1573692024-01-09T09:15:01ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922024-01-011410.3389/fendo.2023.12653721265372Diabetic peripheral neuropathy: pathogenetic mechanisms and treatmentJinxi Zhu0Jinxi Zhu1Ziyan Hu2Ziyan Hu3Yifan Luo4Yinuo Liu5Wei Luo6Xiaohong Du7Zhenzhong Luo8Jialing Hu9Shengliang Peng10Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaThe Second Clinical Medical College of Nanchang University, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaThe Second Clinical Medical College of Nanchang University, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Sports Medicine, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Emergency Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, ChinaDiabetic peripheral neuropathy (DPN) refers to the development of peripheral nerve dysfunction in patients with diabetes when other causes are excluded. Diabetic distal symmetric polyneuropathy (DSPN) is the most representative form of DPN. As one of the most common complications of diabetes, its prevalence increases with the duration of diabetes. 10-15% of newly diagnosed T2DM patients have DSPN, and the prevalence can exceed 50% in patients with diabetes for more than 10 years. Bilateral limb pain, numbness, and paresthesia are the most common clinical manifestations in patients with DPN, and in severe cases, foot ulcers can occur, even leading to amputation. The etiology and pathogenesis of diabetic neuropathy are not yet completely clarified, but hyperglycemia, disorders of lipid metabolism, and abnormalities in insulin signaling pathways are currently considered to be the initiating factors for a range of pathophysiological changes in DPN. In the presence of abnormal metabolic factors, the normal structure and function of the entire peripheral nervous system are disrupted, including myelinated and unmyelinated nerve axons, perikaryon, neurovascular, and glial cells. In addition, abnormalities in the insulin signaling pathway will inhibit neural axon repair and promote apoptosis of damaged cells. Here, we will discuss recent advances in the study of DPN mechanisms, including oxidative stress pathways, mechanisms of microvascular damage, mechanisms of damage to insulin receptor signaling pathways, and other potential mechanisms associated with neuroinflammation, mitochondrial dysfunction, and cellular oxidative damage. Identifying the contributions from each pathway to neuropathy and the associations between them may help us to further explore more targeted screening and treatment interventions.https://www.frontiersin.org/articles/10.3389/fendo.2023.1265372/fulldiabetic peripheral neuropathymolecular mechanismssignal transductiondiagnosistreatment |
| spellingShingle | Jinxi Zhu Jinxi Zhu Ziyan Hu Ziyan Hu Yifan Luo Yinuo Liu Wei Luo Xiaohong Du Zhenzhong Luo Jialing Hu Shengliang Peng Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment Frontiers in Endocrinology diabetic peripheral neuropathy molecular mechanisms signal transduction diagnosis treatment |
| title | Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment |
| title_full | Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment |
| title_fullStr | Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment |
| title_full_unstemmed | Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment |
| title_short | Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment |
| title_sort | diabetic peripheral neuropathy pathogenetic mechanisms and treatment |
| topic | diabetic peripheral neuropathy molecular mechanisms signal transduction diagnosis treatment |
| url | https://www.frontiersin.org/articles/10.3389/fendo.2023.1265372/full |
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