Effects of Brain-Derived Mitochondria on the Function of Neuron and Vascular Endothelial Cell After Traumatic Brain Injury

Zhang, Baoliang; Gao, Yalong; Li, Qifeng; Sun, Dongdong; Dong, Xinlong; Li, Xiaotian; Xin, Wenqiang; Zhang, Jianning

doi:10.1016/j.wneu.2019.11.172

Cited by 16 publications

(18 citation statements)

References 38 publications

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“…Five experimental models targeting brain injury were generated in mice [ 25 ] and rats [ 30 – 33 ], including four focal brain ischemia models (middle cerebral artery occlusion [MCAO]) [ 25 , 31 – 33 ] and one traumatic brain injury (TBI) model [ 30 ]. The types of transplantation used were autologous [ 32 ], allograft [ 25 , 30 ], and xenograft [ 31 , 33 ]. The types of administration were direct or near-direct injection [ 30 – 33 ] and intravenous [ 25 ].…”

Section: Resultsmentioning

confidence: 99%

“…The types of transplantation used were autologous [ 32 ], allograft [ 25 , 30 ], and xenograft [ 31 , 33 ]. The types of administration were direct or near-direct injection [ 30 – 33 ] and intravenous [ 25 ].…”

Section: Resultsmentioning

confidence: 99%

“…TBI is known to result in inflammatory and oxidative stress as well as mitochondrial dysfunction that occurs shortly after the initial impact. Using both a cellular glucose-oxygen deprivation model in bEnd3 and PC12 cells and an in vivo mouse model of TBI using a controlled cortical impact device, Zhang et al [ 30 ] suggested that administration of exogenous brain-derived mitochondria improved cellular respiration and the expression of proteins associated with synaptic plasticity in vitro, along with increased angiogenesis; reduction in apoptosis, brain edema, and blood brain barrier leakage; and improved long-term potentiation in the hippocampus, at 7 days after in vivo TBI.…”

Section: Resultsmentioning

confidence: 99%

“…The types of transplantation used were autologous [32], allograft [25,30], and xenograft [31,33]. The types of administration were direct or near-direct injection [30][31][32][33] and intravenous [25]. Four animal studies demonstrated the benefits of mitochondrial transplantation in the setting of stroke.…”

Section: Brain Iri Modelmentioning

confidence: 99%

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Mitochondrial transplantation therapy for ischemia reperfusion injury: a systematic review of animal and human studies

et al. 2021

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Background Mitochondria are essential organelles that provide energy for cellular functions, participate in cellular signaling and growth, and facilitate cell death. Based on their multifactorial roles, mitochondria are also critical in the progression of critical illnesses. Transplantation of mitochondria has been reported as a potential promising approach to treat critical illnesses, particularly ischemia reperfusion injury (IRI). However, a systematic review of the relevant literature has not been conducted to date. Here, we systematically reviewed the animal and human studies relevant to IRI to summarize the evidence for mitochondrial transplantation. Methods We searched MEDLINE, the Cochrane library, and Embase and performed a systematic review of mitochondrial transplantation for IRI in both preclinical and clinical studies. We developed a search strategy using a combination of keywords and Medical Subject Heading/Emtree terms. Studies including cell-mediated transfer of mitochondria as a transfer method were excluded. Data were extracted to a tailored template, and data synthesis was descriptive because the data were not suitable for meta-analysis. Results Overall, we identified 20 animal studies and two human studies. Among animal studies, 14 (70%) studies focused on either brain or heart IRI. Both autograft and allograft mitochondrial transplantation were used in 17 (85%) animal studies. The designs of the animal studies were heterogeneous in terms of the route of administration, timing of transplantation, and dosage used. Twelve (60%) studies were performed in a blinded manner. All animal studies reported that mitochondrial transplantation markedly mitigated IRI in the target tissues, but there was variation in biological biomarkers and pathological changes. The human studies were conducted with a single-arm, unblinded design, in which autologous mitochondrial transplantation was applied to pediatric patients who required extracorporeal membrane oxygenation (ECMO) for IRI–associated myocardial dysfunction after cardiac surgery. Conclusion The evidence gathered from our systematic review supports the potential beneficial effects of mitochondrial transplantation after IRI, but its clinical translation remains limited. Further investigations are thus required to explore the mechanisms of action and patient outcomes in critical settings after mitochondrial transplantation. Systematic review registration The study was registered at UMIN under the registration number UMIN000043347.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Brain Iri Modelmentioning

confidence: 99%

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Mitochondrial transplantation therapy for ischemia reperfusion injury: a systematic review of animal and human studies

et al. 2021

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“…Mitochondrial supplementation also has shown beneficial effects on restoration of mitochondrial respiratory function [382], as well as on recovery and protection of organs [383,384]. Application of exogenous mitochondria after TBI was found to be protective in vitro and in vivo, which maintained BBB integrity, reduced apoptosis, and improved neurological outcomes [385]. A review article has supported the mitochondrial transplantation as a potentially multifactorial neuroprotective approach after traumatic injuries.…”

Section: Therapeutic Opportunities For Targeting Mitochondria-related...mentioning

confidence: 99%

Oxidative stress and mitochondrial dysfunction following traumatic brain injury: From mechanistic view to targeted therapeutic opportunities

Hakiminia

Alikiaii

Khorvash

et al. 2022

Fundamemntal Clinical Pharma

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Traumatic brain injury (TBI) is one of the most prevalent causes of permanent physical and cognitive disabilities. TBI pathology results from primary insults and a multi-mechanistic biochemical process, termed as secondary brain injury. Currently, there are no pharmacological agents for definitive treatment of patients with TBI. This article is presented with the purpose of reviewing molecular mechanisms of TBI pathology, as well as potential strategies and agents against pathological pathways. In this review article, materials were obtained by searching PubMed, Scopus, Elsevier, Web of Science, and Google Scholar. This search was considered without time limitation. Evidence indicates that oxidative stress and mitochondrial dysfunction are two key mediators of the secondary injury cascade in TBI pathology. TBI-induced oxidative damage results in the structural and functional impairments of cellular and subcellular components, such as mitochondria. Impairments of mitochondrial electron transfer chain and mitochondrial membrane potential result in a vicious cycle of free radical formation and cell apoptosis. The results of some preclinical and clinical studies, evaluating mitochondria-targeted therapies, such as mitochondriatargeted antioxidants and compounds with pleiotropic effects after TBI, are promising. As a proposed strategy in recent years, mitochondria-targeted multipotential therapy is a new hope, waiting to be confirmed. Moreover, based on the available findings, biologics, such as stem cell-based therapy and transplantation of mitochondria are novel potential strategies for the

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Brain microvascular endothelial cell metabolism and its ties to barrier function

Weber,

Moiz,

Clyne

2024

Vitamins and Hormones

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Effects of Brain-Derived Mitochondria on the Function of Neuron and Vascular Endothelial Cell After Traumatic Brain Injury

Cited by 16 publications

References 38 publications

Mitochondrial transplantation therapy for ischemia reperfusion injury: a systematic review of animal and human studies

Mitochondrial transplantation therapy for ischemia reperfusion injury: a systematic review of animal and human studies

Oxidative stress and mitochondrial dysfunction following traumatic brain injury: From mechanistic view to targeted therapeutic opportunities

Brain microvascular endothelial cell metabolism and its ties to barrier function

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