2020
DOI: 10.1038/s41401-020-0449-8
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L-Carnitine protects against tacrolimus-induced renal injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling

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Cited by 25 publications
(20 citation statements)
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“…The distribution of PTEN in podocytes was abnormal, and there was a loss of PTEN distribution in the cell membrane and cytoplasm.After DEX treatment, the above changes could be reversed; furthermore, after PAN damaged podocytes, the expression of the PI3K p85, p-Ak, p-GSK3β and LC3B protein decreased, and the expression of the Bad protein increased. DEX treatment could reverse the changes described above; studies have also found that PTEN may be a kind of protective gene in the kidney [23][24][25][26][27] . High expression of PTEN can negatively regulate the PI3K/Akt pathway, inhibit the activation of Akt, improve the phenotype of renal podocytes, and reduce damage to renal podocytes [28] .In early DN, as glomerular damage increases, the expression of PTEN gradually decreases, suggesting that PTEN has a certain correlation with glomerular damage [29][30][31][32] .…”
Section: Discussionmentioning
confidence: 89%
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“…The distribution of PTEN in podocytes was abnormal, and there was a loss of PTEN distribution in the cell membrane and cytoplasm.After DEX treatment, the above changes could be reversed; furthermore, after PAN damaged podocytes, the expression of the PI3K p85, p-Ak, p-GSK3β and LC3B protein decreased, and the expression of the Bad protein increased. DEX treatment could reverse the changes described above; studies have also found that PTEN may be a kind of protective gene in the kidney [23][24][25][26][27] . High expression of PTEN can negatively regulate the PI3K/Akt pathway, inhibit the activation of Akt, improve the phenotype of renal podocytes, and reduce damage to renal podocytes [28] .In early DN, as glomerular damage increases, the expression of PTEN gradually decreases, suggesting that PTEN has a certain correlation with glomerular damage [29][30][31][32] .…”
Section: Discussionmentioning
confidence: 89%
“…Therefore, some scholars refer to this pathway as the PTEN-PI3K/AKT signal transduction pathway. In recent years, researchers have found that in addition to playing an important role in the eld of tumors, PTEN is also involved in the progression of kidney disease [9][10][11] . Studies have found that in animal models of diabetic nephropathy, the expression of PTEN in glomerular mesangial cells and podocytes is signi cantly downregulated, suggesting that PTEN may play an important role in glomerular sclerosis; in addition, as the expression of PTEN in the kidney is downregulated, podocytes are damaged, and urine protein levels gradually increase [12][13][14] ,suggesting that PTEN may be a protective gene in the kidney.…”
Section: Discussionmentioning
confidence: 99%
“…Either type I (apoptosis) or type II (autophagy) programmed cell death is involved in the pathogenesis of chronic TAC-induced renal injury [ 15 ]. Using TUNEL assay, we observed that most TUNEL-positive cells or apoptotic bodies were localized to tubular epithelia cells and interstitial vascular endothelial cells, where tubular atrophy and typical TIF progressed ( Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Increased proinflammatory mediators in response to injurious stimuli may recruit inflammatory cells, which in turn overexpress proinflammatory and profibrotic cytokines such as chemoattractants, adhesion molecules, and TGF-β1. We have recently demonstrated that NLRP3-dependent and independent inflammasome are involved in the pathogenesis of chronic TAC nephrotoxicity [ 15 ]. Our results show that administering NIC to TAC-treated rats amplifies the expression of pyroptosis-related genes (NLRP3, IL-1β, and IL-18), proinflammatory mediators MCP-1, and profibrotic cytokines TGF-β1 and CTGF, leading to excessive ED-1-positive cells influx and βig-h3 upregulation; these responses reflect the severity of glomerular and tubular injuries.…”
Section: Discussionmentioning
confidence: 99%
“…Many studies were conducted on proximal tubular cells and linked nephrotoxicity either to a mitochondrial toxicity characterized by functional and structural perturbation of the mitochondria (Lim, Shin, Luo, Quan, Cui, et al, 2019; Yu et al, 2019), or to increased oxidative stress caused by an increase of intracellular H 2 O 2 levels or a decrease in MnSOD, an antioxidant enzyme (Lim et al, 2017; Zhou et al, 2004). Autophagy is also found to be disrupted in cells exposed to tacrolimus with an accumulation of autophagy vesicles in the cytoplasm (Lim, Shin, Luo, Quan, Ko, et al, 2019; Zheng et al, 2020). Furthermore, cells exposed to tacrolimus were also found to lose some transporter-related functions (Secker et al, 2019).…”
Section: Introductionmentioning
confidence: 99%