Mi Bai

Publications20
h-index11
Citations326
Highly Influential Citations8
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NLRP3 Inflammasome Mediates Albumin-induced Renal Tubular Injury through Impaired Mitochondrial Function*
Background: The role of NLRP3 inflammasome in albuminuria-induced renal injury and the underlying mechanism remain elusive. Results: Albumin-induced NLRP3 inflammasome activation resulted in the… Expand
  • 60
  • 2
MicroRNA-709 Mediates Acute Tubular Injury through Effects on Mitochondrial Function.
  • Y. Guo, J. Ni, +9 authors A. Zhang
  • Medicine
  • Journal of the American Society of Nephrology…
  • 17 October 2017
Mitochondrial dysfunction has important roles in the pathogenesis of AKI, yet therapeutic approaches to improve mitochondrial function remain limited. In this study, we investigated the pathogenic… Expand
  • 31
  • 2
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Mitochondrial dysfunction confers albumin-induced NLRP3 inflammasome activation and renal tubular injury.
Proteinuria is involved in the development of tubular lesions and in the progressive loss of renal function in chronic kidney diseases via uncertain mechanisms. Growing evidence suggests a pathogenic… Expand
  • 51
  • 1
Dysfunction of the PGC-1α-mitochondria axis confers adriamycin-induced podocyte injury.
Adriamycin (ADR)-induced nephropathy in animals is an experimental analog of human focal segmental glomerulosclerosis, which presents as severe podocyte injury and massive proteinuria and has a… Expand
  • 25
  • 1
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MicroRNA-214 promotes chronic kidney disease by disrupting mitochondrial oxidative phosphorylation.
Mitochondria are critical in determining a cell's energy homeostasis and fate, and mitochondrial dysfunction has been implicated in the pathogenesis of chronic kidney disease (CKD). We sought to… Expand
  • 23
  • 1
MicroRNA-30e targets BNIP3L to protect against aldosterone-induced podocyte apoptosis and mitochondrial dysfunction.
  • Y. Guo, Xu Deng, +8 authors A. Zhang
  • Biology, Medicine
  • American journal of physiology. Renal physiology
  • 1 April 2017
MicroRNAs are essential for the maintenance of podocyte homeostasis. Emerging evidence has demonstrated a protective role of microRNA-30a (miR-30a), a member of the miR-30 family, in podocyte injury.… Expand
  • 11
  • 1
Activation of ERK1/2 by NADPH oxidase-originated reactive oxygen species mediates uric acid-induced mesangial cell proliferation.
Hyperuricemia is associated with kidney complications including glomerulosclerosis and mesangial cell (MC) proliferation by poorly understood mechanisms. The present study investigated the underlying… Expand
  • 26
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NLRP3 inflammasome activation contributes to aldosterone-induced podocyte injury.
  • Mi Bai, Y. Chen, +5 authors A. Zhang
  • Biology, Medicine
  • American journal of physiology. Renal physiology
  • 1 April 2017
Aldosterone (Aldo) has been shown as an important contributor of podocyte injury. However, the underlying molecular mechanisms are still elusive. Recently, the pathogenic role of NOD-like receptor… Expand
  • 16
Angiotensin II Stimulates the NLRP3 Inflammasome to Induce Podocyte Injury and Mitochondrial Dysfunction
Background: We previously reported that the NLRP3 inflammasome played an important role in mediating the podocyte injury induced by aldosterone. However, more studies on the role of the NLRP3… Expand
  • 18
Reactive oxygen species-initiated autophagy opposes aldosterone-induced podocyte injury.
Evidence has demonstrated that aldosterone (Aldo) is involved in the development and progression of chronic kidney diseases. The purpose of the present study was to investigate the role of autophagy… Expand
  • 11
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