Publications by authors named "Pengxi Zheng"

Acute kidney injury (AKI) is a complex renal disease. Long non-coding RNAs (lncRNAs) have frequently been associated with AKI. In the present study, we aimed to investigate the molecular mechanism(s) of LINC00052 in AKI.

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Article Synopsis
  • Diabetic nephropathy (DN) is a serious kidney disease linked to diabetes, where abnormal processes in mesangial cells worsen the condition.
  • The study found that MIAT is up-regulated in DN patients and high glucose-treated mesangial cells, and silencing MIAT reduces abnormal cell growth and fibrosis triggered by high glucose levels.
  • MIAT acts as a sponge for miR-147a, which is reduced in DN, and the loss of MIAT rescues the effects of high glucose, highlighting a pathway where MIAT promotes harmful cell behavior by regulating miR-147a and its target, E2F transcription factor 3 (E2F3).
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The current study aimed to investigate the role and underlying mechanisms of circ_LARP4 in diabetic nephropathy (DN). Here, mouse mesangial cells (SV40-MES13) were cultured with 30 mM glucose to establish a DN cellular model. The qRT-PCR results indicated that circ_LARP4 expression was downregulated in the DN cellular model compared to that in the control cells.

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Recently, microRNAs have been recognized as crucial regulators of diabetic nephropathy (DN) development. Epithelial-to-mesenchymal transition (EMT) can play a significant role in tubulointerstitial fibrosis, and it is a hallmark of diabetic nephropathy progression. Nevertheless, the function of miR-98-5p in the modulation of EMT and renal fibrosis during DN remains barely investigated.

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Long non-coding RNAs (lncRNAs) play vital roles in diabetic nephropathy (DN). This research aimed to study the potential role and underlying molecular mechanisms of long non-coding RNA MEG3 in DN. We found that MEG3 was upregulated in DN in vivo and in vitro and could enhance cell fibrosis and inflammatory response in DN.

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Diabetic nephropathy (DN) is serious diabetic complication with capillary injury. Podocyte injury exerts a crucial effect on DN pathogenesis. MicroRNA-503 (miR-503) has been reported in various diseases including DN.

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