PINK1/Parkin-Mediated Mitophagy Promotes Resistance to Sonodynamic Therapy

Lin, Shiu‐Ru; Huang, Yongjian; Hou, Xuandi; Yang, Yaoheng; Kala, Shashwati; Qiu, Zhihai; Zhang, Rui; Sun, Lei

doi:10.1159/000493629

Cited by 23 publications

(23 citation statements)

References 56 publications

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“…In this review, PS mapping for tumor PDT can be roughly divided into three areas: Mitochondria[ 69 - 78 ], endoplasmic reticulum[ 12 , 68 , 79 - 82 ], and lysosomes[ 83 - 88 ]. These PSs can be roughly summarized into porphyrin-based photosensitizers, such as porphyrins[ 89 - 92 ], chlorins[ 80 , 93 , 94 ], phthalocyanines, and naphthalocyanines[ 95 - 99 ], and non-porphyrin-based photosensitizers, such as cyanine, methylene blue, Nile blue, rhodamine, triarylmethane, and acridine[ 68 , 100 - 105 ]. These PSs and their derivatives are summarized by category in Table 1 .…”

Section: Impact Of Ros From Pdt On Cscsmentioning

confidence: 99%

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Zhang

Wang

et al. 2020

WJSC

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Photodynamic therapy (PDT) is an effective and promising cancer treatment. PDT directly generates reactive oxygen species (ROS) through photochemical reactions. This oxygen-dependent exogenous ROS has anti-cancer stem cell (CSC) effect. In addition, PDT may also increase ROS production by altering metabolism, endoplasmic reticulum stress, or potential of mitochondrial membrane. It is known that the half-life of ROS in PDT is short, with high reactivity and limited diffusion distance. Therefore, the main targeting position of PDT is often the subcellular localization of photosensitizers, which is helpful for us to explain how PDT affects CSC characteristics, including differentiation, self-renewal, apoptosis, autophagy, and immunogenicity. Broadly speaking, excess ROS will damage the redox system and cause oxidative damage to molecules such as DNA, change mitochondrial permeability, activate unfolded protein response, autophagy, and CSC resting state. Therefore, understanding the molecular mechanism by which ROS affect CSCs is beneficial to improve the efficiency of PDT and prevent tumor recurrence and metastasis. In this article, we review the effects of two types of photochemical reactions on PDT, the metabolic processes, and the biological effects of ROS in different subcellular locations on CSCs.

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Section: Impact Of Ros From Pdt On Cscsmentioning

confidence: 99%

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Zhang

Wang

et al. 2020

WJSC

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“…Recent study has found that hepatic fatty acid accumulation can cause damaged mitochondria accumulation, which can impair mitochondrial respiratory chain function and fatty acid oxidative degradation (Ashrafi and Schwarz, 2013; Wu et al, 2015). Surprisingly, PINK1/Parkin-mediated mitophagy can reverse mitochondrial dysfunction and preserve mitochondrial function through eliminating damaged mitochondria in time (Wu et al, 2015; Nguyen et al, 2016; Xiong et al, 2018; Song et al, 2018a; Wang et al, 2019a).…”

Section: Signaling Pathways Involved In Mitophagymentioning

confidence: 99%

Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns

Nie

Huang

et al. 2019

Front. Pharmacol.

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Metabolic syndrome, characterized by central obesity, hypertension, and hyperlipidemia, increases the morbidity and mortality of cardiovascular disease, type 2 diabetes, nonalcoholic fatty liver disease, and other metabolic diseases. It is well known that insulin resistance, especially hepatic insulin resistance, is a risk factor for metabolic syndrome. Current research has shown that hepatic fatty acid accumulation can cause hepatic insulin resistance through increased gluconeogenesis, lipogenesis, chronic inflammation, oxidative stress and endoplasmic reticulum stress, and impaired insulin signal pathway. Mitochondria are the major sites of fatty acid β-oxidation, which is the major degradation mechanism of fatty acids. Mitochondrial dysfunction has been shown to be involved in the development of hepatic fatty acid–induced hepatic insulin resistance. Mitochondrial autophagy (mitophagy), a catabolic process, selectively degrades damaged mitochondria to reverse mitochondrial dysfunction and preserve mitochondrial dynamics and function. Therefore, mitophagy can promote mitochondrial fatty acid oxidation to inhibit hepatic fatty acid accumulation and improve hepatic insulin resistance. Here, we review advances in our understanding of the relationship between mitophagy and hepatic insulin resistance. Additionally, we also highlight the potential value of mitophagy in the treatment of hepatic insulin resistance and metabolic syndrome.

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“…Mitophagy plays an important role in maintaining a healthy population of mitochondria by ensuring that there is an optimal balance between mitochondrial biogenesis and turnover [5,6]. Recently, the involvement of Parkin-mediated mitophagy in nephropathy has come to light [7,8]. In this mitophagy process, Parkin, which is an E3 ubiquitin ligase, is transported from the cytoplasm to depolarized mitochondria, where it subsequently induces the autophagic degradation of dysfunctional mitochondria.…”

mentioning

confidence: 99%

Role of Parkin-mediated mitophagy in the protective effect of polydatin in sepsis-induced acute kidney injury

Gao

Dai

et al. 2020

J Transl Med

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Background: We have reported that polydatin (PD) alleviates mitochondrial dysfunction in rat models of sepsisinduced acute kidney injury (SI-AKI), but the mechanism is not well understood. Here, we investigated the role of Parkin-mediated mitophagy in the protective effects of PD in SI-AKI in mice. Methods: Sepsis was induced in the mice by caecal ligation and puncture. Mitophagy was determined by mitochondrial mass. NLRP3 inflammasome activation was determined by NLRP3, ASC and caspase-1. Mitophagy was blocked by treatment with mitochondrial division inhibitor-1 and Parkin knockout. Key results: PD treatment increased the sepsis-induced loss of mitochondrial mass, indicating the upregulation of mitophagy. Furthermore, PD treatment mediated Parkin translocation from the cytoplasm to the mitochondria. This suggests that Parkin-mediated mitophagy is an underlying mechanism. This was confirmed by the suppression of PD-induced mitophagy in Parkin−/− mice and in mice that were treated with a mitophagy inhibitor. PD-induced Parkin translocation and mitophagy were blocked by inhibiting SIRT1; thus, activation of SIRT1 might be an important molecular mechanism that is triggered by PD. Additionally, PD treatment protected against sepsis-induced kidney injury. These effects were blocked by inhibition of Parkin-dependent mitophagy. Furthermore, PD also protected against mitochondrial dysfunction and mitochondria-dependent apoptosis, and the effect was blocked when Parkindependent mitophagy was inhibited. Finally, PD suppressed NLRP3 inflammasome activation that was also dependent on Parkin-mediated mitophagy. Conclusions: These findings indicate that Parkin-mediated mitophagy is important for the protective effect of PD in SI-AKI, and the underlying mechanisms include the inhibition of mitochondrial dysfunction and NLRP3 inflammasome activation.

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PINK1/Parkin-Mediated Mitophagy Promotes Resistance to Sonodynamic Therapy

Cited by 23 publications

References 56 publications

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns

Role of Parkin-mediated mitophagy in the protective effect of polydatin in sepsis-induced acute kidney injury

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