Role of TFEB in autophagic modulation of ischemia reperfusion injury in mice kidney and protection by urolithin A

Wang, Ying; Huang, Haipeng; Jin, Yuewei; Shen, Kanmin; Chen, Xiaoyi; Xu, Zhijie; Jin, Baiye; Pān, Hào

doi:10.1016/j.fct.2019.110591

Cited by 27 publications

(37 citation statements)

References 56 publications

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“…In renal IR injury, TFEB was translocated to the nucleus and induced lysosomal biogenesis and autophagy. Furthermore, urolithin A treatment enhanced TFEB expression, thus, promoting autophagy and ameliorating renal IR injury [183]. In immunosuppressant tacrolimus (Tac)-induced renal injury, impaired autophagy was found to be in tubules, which exhibited FoxO3-mediated autophagy associated with a reduction of TFEB [184].…”

Section: Tfeb-mediated Autophagy Induction and Renal Injurymentioning

confidence: 99%

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Autophagy Function and Regulation in Kidney Disease

et al. 2020

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Autophagy is a dynamic process by which intracellular damaged macromolecules and organelles are degraded and recycled for the synthesis of new cellular components. Basal autophagy in the kidney acts as a quality control system and is vital for cellular metabolic and organelle homeostasis. Under pathological conditions, autophagy facilitates cellular adaptation; however, activation of autophagy in response to renal injury may be insufficient to provide protection, especially under dysregulated conditions. Kidney-specific deletion of Atg genes in mice has consistently demonstrated worsened acute kidney injury (AKI) outcomes supporting the notion of a pro-survival role of autophagy. Recent studies have also begun to unfold the role of autophagy in progressive renal disease and subsequent fibrosis. Autophagy also influences tubular cell death in renal injury. In this review, we reported the current understanding of autophagy regulation and its role in the pathogenesis of renal injury. In particular, the classic mammalian target of rapamycin (mTOR)-dependent signaling pathway and other mTOR-independent alternative signaling pathways of autophagy regulation were described. Finally, we summarized the impact of autophagy activation on different forms of cell death, including apoptosis and regulated necrosis, associated with the pathophysiology of renal injury. Understanding the regulatory mechanisms of autophagy would identify important targets for therapeutic approaches.

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Section: Tfeb-mediated Autophagy Induction and Renal Injurymentioning

confidence: 99%

“…Renal IR injury Urolithin-A ↑ autophagy by enhanced TFEB expression [183] Tacrolimus-induced renal injury Klotho ↑ autophagy by enhanced nuclear translocation of TFEB [184] Lipopolysaccharide (LPS)-induced podocyte injury…”

Section: Model/ Kidney Disease Agent/drug Effect On Autophagy Referencementioning

confidence: 99%

Autophagy Function and Regulation in Kidney Disease

et al. 2020

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“…Only using 100 mg/kg per day intraperitoneal injection, researchers found that UroA modulated oxidative stress and inflammation caused by cisplatin by reducing pro-inflammatory cytokines, infiltrating leukocytes, and reactive oxygen species production [73]. Within the kidney, UroA induced autophagy, to protect against ischemia-reperfusion injury (IRI) and kidney dysfunction, by decreasing TNFα and IL-1β secretion [74] (Table 3). UroA administration is specified for rodent and human studies; for cell studies, dose is in indicated in μM.…”

Section: Nephrotoxicitymentioning

confidence: 99%

Immunomodulatory Role of Urolithin A on Metabolic Diseases

et al. 2021

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Urolithin A (UroA) is a gut metabolite produced from ellagic acid-containing foods such as pomegranates, berries, and walnuts. UroA is of growing interest due to its therapeutic potential for various metabolic diseases based on immunomodulatory properties. Recent advances in UroA research suggest that UroA administration attenuates inflammation in various tissues, including the brain, adipose, heart, and liver tissues, leading to the potential delay or prevention of the onset of Alzheimer’s disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. In this review, we focus on recent updates of the anti-inflammatory function of UroA and summarize the potential mechanisms by which UroA may help attenuate the onset of diseases in a tissue-specific manner. Therefore, this review aims to shed new insights into UroA as a potent anti-inflammatory molecule to prevent immunometabolic diseases, either by dietary intervention with ellagic acid-rich food or by UroA administration as a new pharmaceutical drug.

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“…Trehalose was confirmed to promote autophagy and attenuate cisplatin-induced AKI through activating TFEB [109]. Urolithin A protects against ischemia/reperfusion-induced renal injury in mice by enhancing TFEBmediated autophagy [110]. Zhang et al [111] found that curcumin has a potential anticancer function by inhibiting mTOR and promoting TFEB nuclear translocation.…”

Section: Drugs Targeting Lysosome Depletionmentioning

confidence: 99%

Lysosome Depletion-Triggered Autophagy Impairment in Progressive Kidney Injury

Chen

Yang

et al. 2021

Kidney Dis

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Background: Macroautophagy (autophagy) is a cellular recycling process involving the destruction of damaged organelles and proteins in intracellular lysosomes for efficient nutrient reuse. Summary: Impairment of the autophagy-lysosome pathway is tightly associated with multiple kidney diseases, such as diabetic nephropathy, proteinuric kidney disease, acute kidney injury, crystalline nephropathy, and drug- and heavy metal-induced renal injury. The impairment in the process of autophagic clearance may induce injury in renal intrinsic cells by activating the inflammasome, inducing cell cycle arrest, and cell death. The lysosome depletion may be a key mechanism triggering this process. In this review, we discuss this pathway and summarize the protective mechanisms for restoration of lysosome function and autophagic flux via the endosomal sorting complex required for transport (ESCRT) machinery, lysophagy, and transcription factor EB-mediated lysosome biogenesis. Key Message: Further exploring mechanisms of ESCRT, lysophagy, and lysosome biogenesis may provide novel therapy strategies for the management of kidney diseases.

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Role of TFEB in autophagic modulation of ischemia reperfusion injury in mice kidney and protection by urolithin A

Cited by 27 publications

References 56 publications

Autophagy Function and Regulation in Kidney Disease

Autophagy Function and Regulation in Kidney Disease

Immunomodulatory Role of Urolithin A on Metabolic Diseases

Lysosome Depletion-Triggered Autophagy Impairment in Progressive Kidney Injury

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