Mitochondria ROS and mitophagy in acute kidney injury

Su, L. Joseph; Zhang, Jiahao; Gómez, Hernando; Kellum, John A.; Peng, Zhiyong

doi:10.1080/15548627.2022.2084862

Cited by 161 publications

(52 citation statements)

References 135 publications

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“…Excessive mtROS promote mitochondrial dysfunction and inflammation leading to mitochondrial damage (Zhao et al, 2021). Mitophagy is an essential mitochondrial quality control mechanism that eliminates damaged mitochondria and the production of ROS (Su et al, 2022). Our study found that iron supplementation can reduce mitochondrial damage and restore ROS levels produced by mitochondria, thereby enhancing the ability of cells to respond to hypoxic stress.…”

Section: Discussionmentioning

confidence: 65%

Iron supplementation inhibits hypoxia-induced mitochondrial damage and protects zebrafish liver cells from death

et al. 2022

Front. Physiol.

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Acute hypoxia in water has always been a thorny problem in aquaculture. Oxygen and iron play important roles and are interdependent in fish. Iron is essential for oxygen transport and its concentration tightly controlled to maintain the cellular redox homeostasis. However, it is still unclear the role and mechanism of iron in hypoxic stress of fish. In this study, we investigated the role of iron in hypoxic responses of two zebrafish-derived cell lines. We found hypoxia exposed zebrafish liver cells (ZFL) demonstrated reduced expression of Ferritin and the gene fth31 for mitochondrial iron storage, corresponding to reduction of both intracellular and mitochondrial free iron and significant decrease of ROS levels in multiple cellular components, including mitochondrial ROS and lipid peroxidation level. In parallel, the mitochondrial integrity was severely damaged. Addition of exogenous iron restored the iron and ROS levels in cellular and mitochondria, reduced mitochondrial damage through enhancing mitophagy leading to higher cell viability, while treated the cells with iron chelator (DFO) or ferroptosis inhibitor (Fer-1) showed no improvements of the cellular conditions. In contrast, in hypoxia insensitive zebrafish embryonic fibroblasts cells (ZF4), the expression of genes related to iron metabolism showed opposite trends of change and higher mitochondrial ROS level compared with the ZFL cells. These results suggest that iron homeostasis is important for zebrafish cells to maintain mitochondrial integrity in hypoxic stress, which is cell type dependent. Our study enriched the hypoxia regulation mechanism of fish, which helped to reduce the hypoxia loss in fish farming.

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Section: Discussionmentioning

confidence: 65%

Iron supplementation inhibits hypoxia-induced mitochondrial damage and protects zebrafish liver cells from death

et al. 2022

Front. Physiol.

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“…Renal perfusion may improve after CPB; however, IRI may subsequently occur and may lead to the opening of mitochondrial permeability transition pores in the kidney [ 64 ], regulating mitophagy [ 65 ] and thereby leading to AKI. IRI can also increase the production of reactive oxygen species (ROS) [ 65 ], which can induce inflammation and promote the occurrence of AKI.…”

Section: Theories Of Csa-aki Pathophysiologymentioning

confidence: 99%

Diagnosis, pathophysiology and preventive strategies for cardiac surgery-associated acute kidney injury: a narrative review

Zhu

et al. 2023

Eur J Med Res

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Acute kidney injury (AKI) is a common and serious complication of cardiac surgery and is associated with increased mortality and morbidity, accompanied by a substantial economic burden. The pathogenesis of cardiac surgery-associated acute kidney injury (CSA-AKI) is multifactorial and complex, with a variety of pathophysiological theories. In addition to the existing diagnostic criteria, the exploration and validation of biomarkers is the focus of research in the field of CSA-AKI diagnosis. Prevention remains the key to the management of CSA-AKI, and common strategies include maintenance of renal perfusion, individualized blood pressure targets, balanced fluid management, goal-directed oxygen delivery, and avoidance of nephrotoxins. This article reviews the pathogenesis, definition and diagnosis, and pharmacological and nonpharmacological prevention strategies of AKI in cardiac surgical patients.

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“…Mitophagy is an important form of selective autophagy that selectively removes excess and defective mitochondria. Research in recent years has proved mitophagy to be a major mechanism underlying the protective effect of autophagy in AKI [ 53 , 54 ]. Mitophagy is mainly mediated by LC3-associated autophagy receptors via ubiquitin (Ub)-dependent and Ub-independent pathways.…”

Section: Reviewmentioning

confidence: 99%

Autophagy in acute kidney injury and maladaptive kidney repair

Xia

et al. 2023

Burns &Amp; Trauma

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Acute kidney injury (AKI) is a major renal disease characterized by a sudden decrease in kidney function. After AKI, the kidney has the ability to repair, but if the initial injury is severe the repair may be incomplete or maladaptive and result in chronic kidney problems. Autophagy is a highly conserved pathway to deliver intracellular contents to lysosomes for degradation. Autophagy plays an important role in maintaining renal function and is involved in the pathogenesis of renal diseases. Autophagy is activated in various forms of AKI and acts as a defense mechanism against kidney cell injury and death. After AKI, autophagy is maintained at a relatively high level in kidney tubule cells during maladaptive kidney repair but the role of autophagy in maladaptive kidney repair has been controversial. Nonetheless, recent studies have demonstrated that autophagy may contribute to maladaptive kidney repair after AKI by inducing tubular degeneration and promoting a profibrotic phenotype in renal tubule cells. In this review, we analyze the role and regulation of autophagy in kidney injury and repair and discuss the therapeutic strategies by targeting autophagy.

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Mitochondria ROS and mitophagy in acute kidney injury

Cited by 161 publications

References 135 publications

Iron supplementation inhibits hypoxia-induced mitochondrial damage and protects zebrafish liver cells from death

Iron supplementation inhibits hypoxia-induced mitochondrial damage and protects zebrafish liver cells from death

Diagnosis, pathophysiology and preventive strategies for cardiac surgery-associated acute kidney injury: a narrative review

Autophagy in acute kidney injury and maladaptive kidney repair

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