New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics
As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and opt...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-08-01
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| Series: | Frontiers in Endocrinology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2023.1230168/full |
| _version_ | 1797739889374003200 |
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| author | Shengnan Wang Haiyang Zhao Suxian Lin Yang Lv Yue Lin Yinai Liu Renyi Peng Huanzhi Jin |
| author_facet | Shengnan Wang Haiyang Zhao Suxian Lin Yang Lv Yue Lin Yinai Liu Renyi Peng Huanzhi Jin |
| author_sort | Shengnan Wang |
| collection | DOAJ |
| description | As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities. |
| first_indexed | 2024-03-12T14:04:41Z |
| format | Article |
| id | doaj.art-51cada3220f84620be108e6c683e1605 |
| institution | Directory Open Access Journal |
| issn | 1664-2392 |
| language | English |
| last_indexed | 2024-03-12T14:04:41Z |
| publishDate | 2023-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj.art-51cada3220f84620be108e6c683e16052023-08-21T15:38:03ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922023-08-011410.3389/fendo.2023.12301681230168New therapeutic directions in type II diabetes and its complications: mitochondrial dynamicsShengnan Wang0Haiyang Zhao1Suxian Lin2Yang Lv3Yue Lin4Yinai Liu5Renyi Peng6Huanzhi Jin7Department of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital, Wenzhou, ChinaInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, ChinaDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital, Wenzhou, ChinaDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital, Wenzhou, ChinaGeneral Practitioner, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital, Wenzhou, ChinaInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, ChinaInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, ChinaGeneral Practitioner, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People’s Hospital, Wenzhou, ChinaAs important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities.https://www.frontiersin.org/articles/10.3389/fendo.2023.1230168/fullmitochondrial dynamicsmitochondrial fusionmitochondrial fissiontype II diabetesdiabetic complications |
| spellingShingle | Shengnan Wang Haiyang Zhao Suxian Lin Yang Lv Yue Lin Yinai Liu Renyi Peng Huanzhi Jin New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics Frontiers in Endocrinology mitochondrial dynamics mitochondrial fusion mitochondrial fission type II diabetes diabetic complications |
| title | New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics |
| title_full | New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics |
| title_fullStr | New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics |
| title_full_unstemmed | New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics |
| title_short | New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics |
| title_sort | new therapeutic directions in type ii diabetes and its complications mitochondrial dynamics |
| topic | mitochondrial dynamics mitochondrial fusion mitochondrial fission type II diabetes diabetic complications |
| url | https://www.frontiersin.org/articles/10.3389/fendo.2023.1230168/full |
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