Sestrin2 attenuates renal damage by regulating Hippo pathway in diabetic nephropathy

Bian, Yawei; Shi, Chonglin; Song, Shan; Lin, Ming Tsan; Wu, Ming; Qiu, Duojun; Dong, Jiajia; Zhang, Wei; Yuan, Chen; Wang, Dongyun; Zhou, Zihui; Xuan, Dong; Shi, Yonghong

doi:10.1007/s00441-022-03668-z

Cited by 11 publications

(10 citation statements)

References 46 publications

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“…A previous study revealed Sestrin2 could suppress YAP activation to regulate cell proliferation and aggravate corneal epithelial damage [16]. Bian et al also demonstrated that Sestrin2 suppressed YAP activation to improve renal damage by regulating Hippo pathway in diabetic nephropathy [17]. Based on the above description, we reasonably conjectured that YAP activation might be implicated in Sestrin2-mediated functions in NSCLC.…”

supporting

confidence: 51%

Sestrin2 mediates FOXM1 expression to block the EMT process in non-small cell lung cancer through the AMPK/YAP pathway

Wang

et al. 2023

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supporting

confidence: 51%

Sestrin2 mediates FOXM1 expression to block the EMT process in non-small cell lung cancer through the AMPK/YAP pathway

Wang

et al. 2023

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“…Besides, Sesn2 -/was associated with podocyte loss and decreased expression of synaptopodin, a marker of differentiated podocytes [98]. Similarly, Bian et al and Song et al indicated that Sestrin2 overexpression could ameliorate renal function and decrease creatinine, blood urea nitrogen, and albuminuria in diabetic mice [62,63]. Overexpression of Sestrin2 also attenuated oxidative stress, reduced transforming growth factor beta (TGF-β) expression, and prevented glomerular hypertrophy, mesangial expansion, and extracellular matrix deposition in diabetic mice in these studies (Figure 3) [62,63].…”

Section: The Beneficial Effects Of Sestrin2 On the Kidney And Diabeti...mentioning

confidence: 89%

“…Sestrin2 overexpression ameliorated oxidative stress in the kidney of diabetic mice associated with both functional and structural improvement [62]. Similarly, Sestrin2 overexpression attenuated oxidative stress in human mesangial cell exposed to high glucose [62].…”

Section: Sestrin2 Ameliorates Oxidative Stress In Diabeticmentioning

confidence: 98%

Section: The Beneficial Effects Of Sestrin2 On the Kidney And Diabeti...mentioning

confidence: 99%

“…In addition to its beneficial effects on podocytes, overexpression of Sestrin2 hindered high glucose-induced mesangial proliferation, production of fibronectin, collagen IV, and ROS in human mesangial cell culture [62]. It was found that Sestrin2 can target Hippo signaling pathway in mesangial cells, thereby alleviating renal fibrosis in diabetic nephropathy [62]. In particular, Sestrin2 overexpression suppressed Yes-associated protein (YAP) and transcription enhancer factor 1 (TEF1) function, whose transcriptional functions are crucial for extracellular matrix protein expression [62].…”

Section: The Beneficial Effects Of Sestrin2 On the Kidney And Diabeti...mentioning

confidence: 99%

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Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy

Ala

2023

Journal of Diabetes Research

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Sestrin2 regulates cell homeostasis and is an upstream signaling molecule for several signaling pathways. Sestrin2 leads to AMP-activated protein kinase- (AMPK-) and GTPase-activating protein activity toward Rags (GATOR) 1-mediated inhibition of mammalian target of rapamycin complex 1 (mTORC1), thereby enhancing autophagy. Sestrin2 also improves mitochondrial biogenesis via AMPK/Sirt1/peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) signaling pathway. Blockade of ribosomal protein synthesis and augmentation of autophagy by Sestrin2 can prevent misfolded protein accumulation and attenuate endoplasmic reticulum (ER) stress. In addition, Sestrin2 enhances P62-mediated autophagic degradation of Keap1 to release nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 release by Sestrin2 vigorously potentiates antioxidant defense in diabetic nephropathy. Impaired autophagy and mitochondrial biogenesis, severe oxidative stress, and ER stress are all deeply involved in the development and progression of diabetic nephropathy. It has been shown that Sestrin2 expression is lower in the kidney of animals and patients with diabetic nephropathy. Sestrin2 knockdown aggravated diabetic nephropathy in animal models. In contrast, upregulation of Sestrin2 enhanced autophagy, mitophagy, and mitochondrial biogenesis and suppressed oxidative stress, ER stress, and apoptosis in diabetic nephropathy. Consistently, overexpression of Sestrin2 ameliorated podocyte injury, mesangial proliferation, proteinuria, and renal fibrosis in animal models of diabetic nephropathy. By suppressing transforming growth factor beta (TGF-β)/Smad and Yes-associated protein (YAP)/transcription enhancer factor 1 (TEF1) signaling pathways in experimental models, Sestrin2 hindered epithelial-mesenchymal transition and extracellular matrix accumulation in diabetic kidneys. Moreover, modulation of the downstream molecules of Sestrin2, for instance, augmentation of AMPK or Nrf2 signaling and inhibition of mTORC1, has been protective in diabetic nephropathy. Regarding the beneficial effects of Sestrin2 on diabetic nephropathy and its interaction with several signaling molecules, it is worth targeting Sestrin2 in diabetic nephropathy.

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One anastomosis gastric bypass ameliorates diabetic nephropathy via regulating the GLP-1-mediated Sirt1/AMPK/PGC1α pathway

Han,

Chen,

Wan

et al. 2024

Clin Exp Nephrol

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Sestrin2 attenuates renal damage by regulating Hippo pathway in diabetic nephropathy

Cited by 11 publications

References 46 publications

Sestrin2 mediates FOXM1 expression to block the EMT process in non-small cell lung cancer through the AMPK/YAP pathway

Sestrin2 mediates FOXM1 expression to block the EMT process in non-small cell lung cancer through the AMPK/YAP pathway

Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy

One anastomosis gastric bypass ameliorates diabetic nephropathy via regulating the GLP-1-mediated Sirt1/AMPK/PGC1α pathway

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