Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury

Chao, Honglu; Lin, Chao; Zuo, Qiang; Liu, Yinlong; Xiao, Mengqing; Xu, Xiupeng; Li, Zheng; Bao, Zhongyuan; Chen, Huimei; You, Yongping; Kochanek, Patrick M.; Yin, Huiyong; Liu, Ning; Kagan, Valerian E.; Bayır, Hülya; Ji, Jing

doi:10.1523/jneurosci.3415-17.2018

Cited by 92 publications

(67 citation statements)

References 58 publications

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“…While cardiolipin, a phospholipid mainly localized at the inner mitochondrial membrane, can externalize to the outer membrane and serve as a mitophagy receptor in neuronal cells (Chu et al, 2013). Cardiolipin mediated mitophagy has been shown to play an important role in traumatic brain injury (TBI) by removing damaged mitochondria thus mitigating ROS overproduction and decreasing apoptosis (Chao et al, 2019).…”

Section: Other Mitophagy Receptorsmentioning

confidence: 99%

Mitophagy: An Emerging Role in Aging and Age-Associated Diseases

Guo

Kroemer

2020

Front. Cell Dev. Biol.

261

159

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Mitochondrial dysfunction constitutes one of the hallmarks of aging and is characterized by irregular mitochondrial morphology, insufficient ATP production, accumulation of mitochondrial DNA (mtDNA) mutations, increased production of mitochondrial reactive oxygen species (ROS) and the consequent oxidative damage to nucleic acids, proteins and lipids. Mitophagy, a mitochondrial quality control mechanism enabling the degradation of damaged and superfluous mitochondria, prevents such detrimental effects and reinstates cellular homeostasis in response to stress. To date, there is increasing evidence that mitophagy is significantly impaired in several human pathologies including aging and age-related diseases such as neurodegenerative disorders, cardiovascular pathologies and cancer. Therapeutic interventions aiming at the induction of mitophagy may have the potency to ameliorate these dysfunctions. In this review, we summarize recent findings on mechanisms controlling mitophagy and its role in aging and the development of human pathologies.

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Section: Other Mitophagy Receptorsmentioning

confidence: 99%

Mitophagy: An Emerging Role in Aging and Age-Associated Diseases

Guo

Kroemer

2020

Front. Cell Dev. Biol.

261

159

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“…Mitochondria are indispensable organelles for energy production, cell signaling, and cell survival in eukaryotic cells. However, damaged and dysfunctional mitochondria are also responsible for generating the majority of reactive oxygen species (ROS) and the release of cytochrome c (cyt c), which results in cell death 12 . Thus selective elimination of damaged mitochondria by mitophagy could be a potential therapeutic target for TBI.…”

Section: Introductionmentioning

confidence: 99%

Dual effects of thyroid hormone on neurons and neurogenesis in traumatic brain injury

Lin

Chang

et al. 2020

Cell Death Dis

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Thyroid hormone (TH) plays a crucial role in neurodevelopment, but its function and specific mechanisms remain unclear after traumatic brain injury (TBI). Here we found that treatment with triiodothyronine (T3) ameliorated the progression of neurological deficits in mice subjected to TBI. The data showed that T3 reduced neural death and promoted the elimination of damaged mitochondria via mitophagy. However, T3 did not prevent TBI-induced cell death in phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (Pink1) knockout mice suggesting the involvement of mitophagy. Moreover, we also found that T3 promoted neurogenesis via crosstalk between mature neurons and neural stem cells (NSCs) after TBI. In neuron cultures undergoing oxygen and glucose deprivation (OGD), conditioned neuron culture medium collected after T3 treatment enhanced the in vitro differentiation of NSCs into mature neurons, a process in which mitophagy was required. Taken together, these data suggested that T3 treatment could provide a therapeutic approach for TBI by preventing neuronal death via mitophagy and promoting neurogenesis via neuron–NSC crosstalk.

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“…The importance of CL externalization as a signal to degrade damaged mitochondria via autophagy has been demonstrated in vitro and in vivo [16,18,22,31]. In this work, LC3A has been identified as an additional LC3 family member involved in mitophagy, and key residues for its interaction with CL have been singled out.…”

Section: Discussionmentioning

confidence: 88%

“…Recent studies have demonstrated that CL-externalization takes place also in vivo. Traumatic Brain Injury (TBI) model animals externalize CL to the OMM to a similar extent than rotenone-exposed mitochondria, thus underlining the importance of CL for mitophagy induction during the early response to this injury in human and rat brain [18]. Moreover, it is known that taffazin-deficiency related perturbations in CL remodeling related to Barth syndrome cause defective mitophagosome biogenesis [19].…”

Section: Introductionmentioning

confidence: 99%

LC3 subfamily in cardiolipin-mediated mitophagy: A comparison of the LC3A, LC3B and LC3C homologs

Etxaniz

Varela

Hervás

et al. 2020

Preprint

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Among the described indicators of mitochondrial damage, externalization of the phospholipid cardiolipin (CL) to the outer mitochondrial membrane has been proposed to trigger mitophagy, acting as a signal for binding the autophagy protein LC3B. However, the behavior of the other LC3 subfamily members has not been explored yet. In the present contribution, a comparative analysis of the interaction of LC3B, LC3A and LC3C with CL-containing model membranes, as well as their ability to translocate to mitochondria was assessed. Binding of LC3A to CL was higher than that of LC3B, and both proteins showed a similar ability to colocalize with mitochondria upon induction of CL externalization by rotenone in HeLa-NDPK-D or SH-SY5Y cells. Two residues located in the N-terminal region of LC3A were shown to be important for its recognition of damaged mitochondria. Moreover, the in vitro results suggested a possible role of LC3A, but not of LC3B, in oxidized-CL recognition as a counterweight to excessive apoptosis activation. In the case of LC3C, even if this protein showed a higher binding than LC3B or LC3A to CL, binding was less specific, and colocalization of LC3C with mitochondria was not rotenone-dependent. These results suggest that, at variance with LC3A, LC3C does not participate in the rotenone-CL mitophagy mechanism. The data support the notion that the various LC3/GABARAP family members might play different roles during autophagy initiation, identifying LC3A as a novel stakeholder in CL-mediated mitophagy.

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Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury

Cited by 92 publications

References 58 publications

Mitophagy: An Emerging Role in Aging and Age-Associated Diseases

Mitophagy: An Emerging Role in Aging and Age-Associated Diseases

Dual effects of thyroid hormone on neurons and neurogenesis in traumatic brain injury

LC3 subfamily in cardiolipin-mediated mitophagy: A comparison of the LC3A, LC3B and LC3C homologs

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