Activation of PINK1/Parkin-mediated mitophagy protects against apoptosis in kidney damage caused by aluminum

Liu, Pengli; Cui, Yilong; Zhang, Xuliang; Xiao, Bonan; Liu, Meilin; Song, Miao; Li, Yanfei

doi:10.1016/j.jinorgbio.2022.111765

Cited by 9 publications

(3 citation statements)

References 52 publications

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“…Our findings confirmed that ER stress-induced mitophagy protected germ cells from MEHP exposure-induced death, similar to the protective role documented in other toxicity studies. 58 , 59 Consistent with the findings of our previous study, pyroptosis was also observed in these cells. Moreover, 4-PBA rescued MEHP-injured germ cells undergoing pyroptosis.…”

Section: Discussionsupporting

confidence: 92%

X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl) phthalate-induced testis toxicity

Hong¹,

Zhou²,

Li³

et al. 2024

Genes & Diseases

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Section: Discussionsupporting

confidence: 92%

X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl) phthalate-induced testis toxicity

Hong¹,

Zhou²,

Li³

et al. 2024

Genes & Diseases

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“…However, when CsA was administered to inhibit mitophagy, apoptosis increased. Liu et al demonstrated that the PINK1-/parkin-mediated mitophagy offers protection against apoptosis in aluminum-induced kidney damage ( 11 ), Hu et al demonstrated that Sal B protects against myocardial ischemic injury by enhancing mitophagy and sustaining mitochondrial activity ( 48 ), and Jiang et al demonstrated that PINK1-/parkin-mediated mitophagy reduces palmitic acid-induced apoptosis by minimizing mitochondrial ROS formation ( 12 ). Our findings indicate that the activation of PINK1-/parkin-mediated mitophagy protects against apoptosis in kidney damage caused by IR.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequently, caspase-9 is cleaved and activated, which then activates the key effector protein in the apoptosis protease cascade, caspase-3 ( 9 , 10 ). Evidence suggests that enhanced apoptosis severely injures the kidney and renders it dysfunctional ( 5 , 11 ). Kidneys are often rich in mitochondria due to their high metabolic requirements and the need to detect and respond to oxidative stress and inflammation generated by injuries.…”

Section: Introductionmentioning

confidence: 99%

Suppression of NLRP3 inflammasome activation by astragaloside IV via promotion of mitophagy to ameliorate radiation-induced renal injury in mice

Ding,

Liu,

Zhang

et al. 2024

Transl Androl Urol

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Background Irradiation (IR) promotes inflammation and apoptosis by inducing oxidative stress and/or mitochondrial dysfunction (MD). The kidneys are rich in mitochondria, and mitophagy maintains normal renal function by eliminating damaged mitochondria and minimizing oxidative stress. However, whether astragaloside IV (AS-IV) can play a protective role through the mitophagy pathway is not known. Methods We constructed a radiation injury model using hematoxylin and eosin (HE) staining, blood biochemical analysis, immunohistochemistry, TdT-mediated dUTP nick end labeling (TUNEL) staining, ultrastructural observation, and Western blot analysis to elucidate the AS-IV resistance mechanism for IR-induced renal injury. Results IR induced mitochondrial damage; the increase of creatinine (SCr), blood urea nitrogen (BUN) and uric acid (UA); and the activation of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome and apoptosis in renal tissue. AS-IV administration attenuated the IR-induced MD and reactive oxygen species (ROS) levels in the kidney; enhanced the levels of mitophagy-associated protein [PTEN-induced putative kinase 1 (PINK1)], parkin proteins, and microtubule-associated protein 1 light 3 (LC3) II/I ratio in renal tissues; diminished NLRP3 inflammasome activation-mediated proteins [cleaved cysteinyl aspartate-specific proteinase-1 (caspase-1), interleukin-1β (IL-1β)] and apoptosis-related proteins [cleaved caspase-9, cleaved caspase-3, BCL2-associated X (Bax)]; reduced SCr, BUN, and UA levels; and attenuated the histopathological alterations in renal tissue. Conversely, mitophagy inhibitor cyclosporin A (CsA) suppressed the AS-IV-mediated protection of renal tissue. Conclusions AS-IV can strongly diminish the activation and apoptosis of NLRP3 inflammasome, thus attenuating the renal injury induced by radiation by promoting the PINK1/parkin-mediated mitophagy. These findings suggest that AS-IV is a promising drug for treating IR-induced kidney injury.

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Restoration of metal homeostasis: a potential strategy against neurodegenerative diseases

Zhang

Ren

et al. 2023

Ageing Research Reviews

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Activation of PINK1/Parkin-mediated mitophagy protects against apoptosis in kidney damage caused by aluminum

Cited by 9 publications

References 52 publications

X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl) phthalate-induced testis toxicity

X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl) phthalate-induced testis toxicity

Suppression of NLRP3 inflammasome activation by astragaloside IV via promotion of mitophagy to ameliorate radiation-induced renal injury in mice

Restoration of metal homeostasis: a potential strategy against neurodegenerative diseases

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