Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies
This systematic review sought to determine the effects of Mitochondrial division inhibitor-1 (Mdivi-1) on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in ischemia/reperfusion (I/R) injury after ischemic stroke. Pubmed, Web of Science, and EMBASE databases were searched...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2021-12-01
|
| Series: | Frontiers in Molecular Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fnmol.2021.778569/full |
| _version_ | 1818966237209690112 |
|---|---|
| author | Nguyen Thanh Nhu Qing Li Yijie Liu Jian Xu Shu-Yun Xiao Shin-Da Lee Shin-Da Lee Shin-Da Lee |
| author_facet | Nguyen Thanh Nhu Qing Li Yijie Liu Jian Xu Shu-Yun Xiao Shin-Da Lee Shin-Da Lee Shin-Da Lee |
| author_sort | Nguyen Thanh Nhu |
| collection | DOAJ |
| description | This systematic review sought to determine the effects of Mitochondrial division inhibitor-1 (Mdivi-1) on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in ischemia/reperfusion (I/R) injury after ischemic stroke. Pubmed, Web of Science, and EMBASE databases were searched through July 2021. The studies published in English language that mentioned the effects of Mdivi-1 on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in I/R-induced brain injury were included. The CAMARADES checklist (for in vivo studies) and the TOXRTOOL checklist (for in vitro studies) were used for study quality evaluation. Twelve studies were included (median CAMARADES score = 6; TOXRTOOL scores ranging from 16 to 18). All studies investigated neural mitochondrial functions, providing that Mdivi-1 attenuated the mitochondrial membrane potential dissipation, ATP depletion, and complexes I-V abnormalities; enhanced mitochondrial biogenesis, as well as inactivated mitochondrial fission and mitophagy in I/R-induced brain injury. Ten studies analyzed neural mitochondria-mediated apoptosis, showing that Mdivi-1 decreased the levels of mitochondria-mediated proapoptotic factors (AIF, Bax, cytochrome c, caspase-9, and caspase-3) and enhanced the level of antiapoptotic factor (Bcl-2) against I/R-induced brain injury. The findings suggest that Mdivi-1 can protect neural mitochondrial functions, thereby attenuating neural mitochondria-mediated apoptosis in I/R-induced brain injury. Our review supports Mdivi-1 as a potential therapeutic compound to reduce brain damage in ischemic stroke (PROSPERO protocol registration ID: CRD42020205808).Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/], identifier [CRD42020205808]. |
| first_indexed | 2024-12-20T13:29:42Z |
| format | Article |
| id | doaj.art-431c4d49bd904c80bd4cb696e3760698 |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-12-20T13:29:42Z |
| publishDate | 2021-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-431c4d49bd904c80bd4cb696e37606982022-12-21T19:39:08ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992021-12-011410.3389/fnmol.2021.778569778569Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical StudiesNguyen Thanh Nhu0Qing Li1Yijie Liu2Jian Xu3Shu-Yun Xiao4Shin-Da Lee5Shin-Da Lee6Shin-Da Lee7Faculty of Medicine, Can Tho University of Medicine and Pharmacy, Can Tho, VietnamDepartment of Rehabilitation, Shanghai Xuhui Central Hospital/Zhongshan-Xuhui Hospital, Fudan University, Shanghai, ChinaInstitute of Rehabilitation Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Brain and Mental Disease, Shanghai Hospital of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Brain and Mental Disease, Shanghai Hospital of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Physical Therapy, Graduate Institute of Rehabilitation Science, China Medical University, Taichung, TaiwanDepartment of Physical Therapy, Asia University, Taichung, TaiwanSchool of Rehabilitation Medicine, Weifang Medical University, Weifang, ChinaThis systematic review sought to determine the effects of Mitochondrial division inhibitor-1 (Mdivi-1) on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in ischemia/reperfusion (I/R) injury after ischemic stroke. Pubmed, Web of Science, and EMBASE databases were searched through July 2021. The studies published in English language that mentioned the effects of Mdivi-1 on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in I/R-induced brain injury were included. The CAMARADES checklist (for in vivo studies) and the TOXRTOOL checklist (for in vitro studies) were used for study quality evaluation. Twelve studies were included (median CAMARADES score = 6; TOXRTOOL scores ranging from 16 to 18). All studies investigated neural mitochondrial functions, providing that Mdivi-1 attenuated the mitochondrial membrane potential dissipation, ATP depletion, and complexes I-V abnormalities; enhanced mitochondrial biogenesis, as well as inactivated mitochondrial fission and mitophagy in I/R-induced brain injury. Ten studies analyzed neural mitochondria-mediated apoptosis, showing that Mdivi-1 decreased the levels of mitochondria-mediated proapoptotic factors (AIF, Bax, cytochrome c, caspase-9, and caspase-3) and enhanced the level of antiapoptotic factor (Bcl-2) against I/R-induced brain injury. The findings suggest that Mdivi-1 can protect neural mitochondrial functions, thereby attenuating neural mitochondria-mediated apoptosis in I/R-induced brain injury. Our review supports Mdivi-1 as a potential therapeutic compound to reduce brain damage in ischemic stroke (PROSPERO protocol registration ID: CRD42020205808).Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/], identifier [CRD42020205808].https://www.frontiersin.org/articles/10.3389/fnmol.2021.778569/fullMdivi-1mitochondrial functionapoptosisischemia-reperfusion injurystroke |
| spellingShingle | Nguyen Thanh Nhu Qing Li Yijie Liu Jian Xu Shu-Yun Xiao Shin-Da Lee Shin-Da Lee Shin-Da Lee Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies Frontiers in Molecular Neuroscience Mdivi-1 mitochondrial function apoptosis ischemia-reperfusion injury stroke |
| title | Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies |
| title_full | Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies |
| title_fullStr | Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies |
| title_full_unstemmed | Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies |
| title_short | Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies |
| title_sort | effects of mdivi 1 on neural mitochondrial dysfunction and mitochondria mediated apoptosis in ischemia reperfusion injury after stroke a systematic review of preclinical studies |
| topic | Mdivi-1 mitochondrial function apoptosis ischemia-reperfusion injury stroke |
| url | https://www.frontiersin.org/articles/10.3389/fnmol.2021.778569/full |
| work_keys_str_mv | AT nguyenthanhnhu effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT qingli effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT yijieliu effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT jianxu effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT shuyunxiao effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT shindalee effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT shindalee effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies AT shindalee effectsofmdivi1onneuralmitochondrialdysfunctionandmitochondriamediatedapoptosisinischemiareperfusioninjuryafterstrokeasystematicreviewofpreclinicalstudies |