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Original Articles

Decreasing REDD1 expression protects against high glucose-induced apoptosis, oxidative stress and inflammatory injury in podocytes through regulation of the AKT/GSK-3β/Nrf2 pathway

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Pages 527-538 | Received 09 Jul 2022, Accepted 10 Feb 2023, Published online: 07 Mar 2023

References

  • Harjutsalo V, Groop PH. Epidemiology and risk factors for diabetic kidney disease. Adv Chronic Kidney Dis. 2014;21(3):260–266.
  • Gheith O, Farouk N, Nampoory N, et al. Diabetic kidney disease: world wide difference of prevalence and risk factors. J Nephropharmacol. 2016;5(1):49–56.
  • Shankland SJ. The podocyte’s response to injury: role in proteinuria and glomerulosclerosis. Kidney Int. 2006;69(12):2131–2147.
  • Mundel P, Shankland SJ. Podocyte biology and response to injury. J Am Soc Nephrol. 2002;13(12):3005–3015.
  • Jha JC, Banal C, Chow BS, et al. Diabetes and kidney disease: role of oxidative stress. Antioxid Redox Signal. 2016;25(12):657–684.
  • Koch EAT, Nakhoul R, Nakhoul F, et al. Autophagy in diabetic nephropathy: a review. Int Urol Nephrol. 2020;52(9):1705–1712.
  • Britto FA, Dumas K, Giorgetti-Peraldi S, et al. Is REDD1 a metabolic double agent? Lessons from physiology and pathology. Am J Physiol Cell Physiol. 2020;319(5):C807–C824.
  • Shoshani T, Faerman A, Mett I, et al. Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis. Mol Cell Biol. 2002;22(7):2283–2293.
  • Ellisen LW, Ramsayer KD, Johannessen CM, et al. REDD1, a developmentally regulated transcriptional target of p63 and p53, links p63 to regulation of reactive oxygen species. Mol Cell. 2002; 10(5):995–1005.
  • Wang Z, Malone MH, Thomenius MJ, et al. Dexamethasone-induced gene 2 (dig2) is a novel pro-survival stress gene induced rapidly by diverse apoptotic signals. J Biol Chem. 2003;278(29):27053–27058.
  • Sofer A, Lei K, Johannessen CM, et al. Regulation of mTOR and cell growth in response to energy stress by REDD1. Mol Cell Biol. 2005;25(14):5834–5845.
  • Lee DK, Kim JH, Kim J, et al. REDD-1 aggravates endotoxin-induced inflammation via atypical NF-kappaB activation. Faseb J. 2018;32(8):4585–4599.
  • Su J, Wang M, Yan Y, et al. Increased REDD1 facilitates neuronal damage after subarachnoid hemorrhage. Neurochem Int. 2019;128:14–20.
  • Sun J, Yue F. Suppression of REDD1 attenuates oxygen glucose deprivation/reoxygenation-evoked ischemic injury in neuron by suppressing mTOR-mediated excessive autophagy. J Cell Biochem. 2019;120(9):14771–14779.
  • Pastor F, Dumas K, Barthelemy MA, et al. Implication of REDD1 in the activation of inflammatory pathways. Sci Rep. 2017;7(1):7023.
  • Tirado-Hurtado I, Fajardo W, Pinto JA. DNA damage inducible transcript 4 gene: the switch of the metabolism as potential target in cancer. Front Oncol. 2018;8:106.
  • Malagelada C, Ryu EJ, Biswas SC, et al. RTP801 is elevated in parkinson brain substantia nigral neurons and mediates death in cellular models of parkinson’s disease by a mechanism involving mammalian target of rapamycin inactivation. J Neurosci. 2006;26(39):9996–10005.
  • McGhee NK, Jefferson LS, Kimball SR. Elevated corticosterone associated with food deprivation upregulates expression in rat skeletal muscle of the mTORC1 repressor, REDD1. J Nutr. 2009;139(5):828–834.
  • Itoh K, Mimura J, Yamamoto M. Discovery of the negative regulator of Nrf2, Keap1: a historical overview. Antioxid Redox Signal. 2010;13(11):1665–1678.
  • Kensler TW, Wakabayashi N, Biswal S. Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. Annu Rev Pharmacol Toxicol. 2007;47:89–116.
  • Silva-Islas CA, Maldonado PD. Canonical and non-canonical mechanisms of Nrf2 activation. Pharmacol Res. 2018;134:92–99.
  • Rojo AI, Medina-Campos ON, Rada P, et al. Signaling pathways activated by the phytochemical nordihydroguaiaretic acid contribute to a Keap1-independent regulation of Nrf2 stability: role of glycogen synthase kinase-3. Free Radic Biol Med. 2012;52(2):473–487.
  • Rada P, Rojo AI, Chowdhry S, et al. SCF/{beta}-TrCP promotes glycogen synthase kinase 3-dependent degradation of the Nrf2 transcription factor in a Keap1-independent manner. Mol Cell Biol. 2011;31(6):1121–1133.
  • Li YC, Gao WJ. GSK-3beta activity and hyperdopamine-dependent behaviors. Neurosci Biobehav Rev. 2011;35(3):645–654.
  • Fao L, Mota SI, Rego AC. Shaping the Nrf2-ARE-related pathways in alzheimer’s and parkinson’s diseases. Ageing Res Rev. 2019;54:100942.
  • Liu WJ, Reiser J, Park TS, et al. New insights into diabetic kidney disease: the potential pathogenesis and therapeutic targets. J Diabetes Res. 2017;2017:3945469.
  • Rush BM, Bondi CD, Stocker SD, et al. Genetic or pharmacologic Nrf2 activation increases proteinuria in chronic kidney disease in mice. Kidney Int. 2021;99:(1):102–116.
  • Hulmi JJ, Silvennoinen M, Lehti M, et al. Altered REDD1, myostatin, and akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy. Am J Physiol Endocrinol Metab. 2012;302(3):E307–E315.
  • Dennis MD, Kimball SR, Fort PE, et al. Regulated in development and DNA damage 1 is necessary for hyperglycemia-induced vascular endothelial growth factor expression in the retina of diabetic rodents. J Biol Chem. 2015; 290(6):3865–3874.
  • Cui FQ, Wang YF, Gao YB, et al. Effects of BSF on podocyte apoptosis via regulating the ROS-Mediated PI3K/AKT pathway in DN. J Diabetes Res. 2019;2019:9512406.
  • Zhu L, Han J, Yuan R, et al. Berberine ameliorates diabetic nephropathy by inhibiting TLR4/NF-kappaB pathway. Biol Res. 2018;51(1):9.
  • Miller WP, Yang C, Mihailescu ML, et al. Deletion of the akt/mTORC1 repressor REDD1 prevents visual dysfunction in a rodent model of type 1 diabetes. Diabetes. 2018;67(1):110–119.
  • Miller WP, Toro AL, Barber AJ, et al. REDD1 activates a ROS-generating feedback loop in the retina of diabetic mice. Invest Ophthalmol Vis Sci. 2019;60(6):2369–2379.
  • Yoshida T, Mett I, Bhunia AK, et al. Rtp801, a suppressor of mTOR signaling, is an essential mediator of cigarette smoke-induced pulmonary injury and emphysema. Nat Med. 2010; 16(7):767–773.
  • Yin H, Zhang Y, Wang K, et al. The involvement of regulated in development and DNA damage response 1 (REDD1) in the pathogenesis of intervertebral disc degeneration. Exp Cell Res. 2018;372(2):188–197.
  • Li P, Lin N, Guo M, et al. REDD1 knockdown protects H9c2 cells against myocardial ischemia/reperfusion injury through akt/mTORC1/Nrf2 pathway-ameliorated oxidative stress: an in vitro study. Biochem Biophys Res Commun. 2019;519(1):179–185.
  • Miller WP, Sunilkumar S, Giordano JF, et al. The stress response protein REDD1 promotes diabetes-induced oxidative stress in the retina by Keap1-independent Nrf2 degradation. J Biol Chem. 2020;295(21):7350–7361.
  • Gu Y, Kaufman JL, Bernal L, et al. MLN4924, an NAE inhibitor, suppresses AKT and mTOR signaling via upregulation of REDD1 in human myeloma cells. Blood. 2014;123(21):3269–3276.
  • Dennis MD, Coleman CS, Berg A, et al. REDD1 enhances protein phosphatase 2A-mediated dephosphorylation of akt to repress mTORC1 signaling. Sci Signal. 2014;7(335):ra68.
  • Favier FB, Costes F, Defour A, et al. Downregulation of akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia. Am J Physiol Regul Integr Comp Physiol. 2010;298(6):R1659–R1666.
  • Paeng J, Chang JH, Lee SH, et al. Enhanced glycogen synthase kinase-3beta activity mediates podocyte apoptosis under diabetic conditions. Apoptosis. 2014;19(12):1678–1690.
  • Zhang C, Hou B, Yu S, et al. HGF alleviates high glucose-induced injury in podocytes by GSK3beta inhibition and autophagy restoration. Biochim Biophys Acta. 2016;1863(11):2690–2699.
  • Chen Z, Tian L, Wang L, et al. TRIM32 inhibition attenuates apoptosis, oxidative stress, and inflammatory injury in podocytes induced by high glucose by modulating the akt/GSK-3beta/Nrf2 pathway. Inflammation. 2022;45(3):992–1006.
  • Liu C, Li Y, Wang X. TDAG51-Deficiency podocytes are protected from High-Glucose-Induced damage through Nrf2 activation via the AKT-GSK-3beta pathway. Inflammation. 2022;17:1520–1533.
  • Rushworth SA, Shah S, MacEwan DJ. TNF mediates the sustained activation of Nrf2 in human monocytes. J Immunol. 2011;187(2):702–707.
  • Xu E, Yin C, Yi X, et al. Inhibition of USP15 ameliorates high-glucose-induced oxidative stress and inflammatory injury in podocytes through regulation of the Keap1/Nrf2 signaling. Environ Toxicol. 2022;37(4):765–775.
  • Liu C, Li Y, Wang X. TDAG51-Deficiency podocytes are protected from High-Glucose-Induced damage through Nrf2 activation via the AKT-GSK-3beta pathway. Inflammation. 2022;45(4):1520–1533.

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