Defective mitophagy and induction of apoptosis by the depleted levels of PINK1 and Parkin in Pb and β-amyloid peptide induced toxicity

Bandaru, Lakshmi Jaya Madhuri; Ayyalasomayajula, Neelima; Murumulla, Lokesh; Dixit, Prasanna Kumar; Challa, Suresh

doi:10.1080/15376516.2022.2054749

Cited by 10 publications

(2 citation statements)

References 42 publications

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“…PINK1 is, under physiological conditions, present in low levels in the OMM. When there is damage to the mitochondria/loss of mitochondrial membrane potential, PINK1 is stabilized in the OMM [37]. Accumulated PINK1 autophosphorylates, followed by ubiquitin phosphorylation, recruiting Parkin to the mitochondrial membrane.…”

Section: Mitophagymentioning

confidence: 99%

Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials

Luan

Jiang

Luan

et al. 2023

Oxidative Medicine and Cellular Longevity

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Traumatic brain injury (TBI), a kind of external trauma-induced brain function alteration, has posed a financial burden on the public health system. TBI pathogenesis involves a complicated set of events, including primary and secondary injuries that can cause mitochondrial damage. Mitophagy, a process in which defective mitochondria are specifically degraded, segregates and degrades defective mitochondria allowing a healthier mitochondrial network. Mitophagy ensures that mitochondria remain healthy during TBI, determining whether neurons live or die. Mitophagy acts as a critical regulator in maintaining neuronal survival and healthy. This review will discuss the TBI pathophysiology and the consequences of the damage it causes to mitochondria. This review article will explore the mitophagy process, its key factors, and pathways and reveal the role of mitophagy in TBI. Mitophagy will be further recognized as a therapeutic approach in TBI. This review will offer new insights into mitophagy’s role in TBI progression.

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Section: Mitophagymentioning

confidence: 99%

Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials

Luan

Jiang

Luan

et al. 2023

Oxidative Medicine and Cellular Longevity

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“…In malignant tumors, mitophagy involves abnormal activation and proliferation of cancer cells. Inhibition of mitophagy in cancer cells to exert tumorsuppressing effect [9] , and enhance mitophagy in normal cells to remove damaged mitochondria, maintain mitochondrial genome stability and normal function, and thus exert oncogenic effect [10] .…”

Section: Introductionmentioning

confidence: 99%

Therapeutic effect of V8 affecting mitophagy and endoplasmic reticulum stress in acute myeloid leukemia mediated by ROS and CHOP signaling

Hui

Guo

Zhu

et al. 2023

Preprint

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Acute myeloid leukemia (AML) is a disease of malignant proliferation of abnormally or poorly differentiated myeloid cells of the hematopoietic system. The clinical treatments of non-M3 AML are experiencing a lack of effective drugs. V8 is a newly synthesized derivative of the natural flavonoid wogonin, which belongs to the potential anticancer drug, and has shown significant antitumor activity in vitro and in vivo. In this study, we investigated the effects of V8 on AML cell lines and primary AML cells and the underlying mechanisms. The results showed that V8 inhibited the growth and induced the apoptosis of AML cell lines (ME-1, Kasumi-1, and U937) and primary AML cells in a concentration-dependent manner. Meanwhile, we revealed that V8-induced apoptosis was accompanied by mitochondrial injury, such as the reduction of mitochondrial membrane potential and ATP production, activation of endoplasmic reticulum stress (ERS) characterized by GRP78 and caspase-12 expression upregulation. Mechanism studies have shown that V8 induced mitochondrial injury and inhibited mitophagy via elevating the intracellular ROS level. In addition, V8 activated PERK-p-eIF2α-ATF4 and Ire1α-XBP1 pathways and induced apoptosis of AML cells via selectively activating CHOP. Correspondingly, the degree of apoptosis and expression of apoptosis-related proteins were alleviated after the elimination of cytoplasmic ROS with N-Acetyl-L-cysteine (NAC) and knocking out CHOP in the cells by transfection with CHOP shRNA, implicating that mitochondrial injury-triggered upregulation of ROS and CHOP played an important role in V8-induced apoptosis of AML cells. In primary AML cells-bearing NOD/SCID mice model and U937 cells-inoculating BALB/c nude mice xenografts transplantation tumor model, administration of V8 markedly prolonged survival time and inhibited the xenografts growth via CHOP-mediated ERS in vivo. In conclusion, our study provides a new insight into the mechanism of V8-induced apoptosis, suggesting the potential of V8 as a promising agent against AML.

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Exposure of combination of environmental pollutant, lead (Pb) and β-amyloid peptides causes mitochondrial dysfunction and oxidative stress in human neuronal cells

Bandaru

Murumulla

et al. 2023

J Bioenerg Biomembr

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Defective mitophagy and induction of apoptosis by the depleted levels of PINK1 and Parkin in Pb and β-amyloid peptide induced toxicity

Cited by 10 publications

References 42 publications

Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials

Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials

Therapeutic effect of V8 affecting mitophagy and endoplasmic reticulum stress in acute myeloid leukemia mediated by ROS and CHOP signaling

Exposure of combination of environmental pollutant, lead (Pb) and β-amyloid peptides causes mitochondrial dysfunction and oxidative stress in human neuronal cells

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