Results 51 to 60 of about 899,728 (258)

USP30‐Mediated Deubiquitination of PEX5 Suppresses Pexophagy to Drive Tubular Injury in Diabetic Kidney Disease

open access: yesAdvanced Science, EarlyView.
USP30 accumulation in diabetic renal tubular epithelial cells deubiquitinates PEX5, suppresses pexophagy, and drives dysfunctional peroxisome accumulation and tubular injury. USP30 depletion restores PEX5 ubiquitination and pexophagy, improves peroxisomal function, and alleviates tubular damage, highlighting USP30 as a therapeutic target in diabetic ...
Jia Li   +10 more
wiley   +1 more source

Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration

open access: yesJCI Insight, 2021
The transcription factor Twist1 regulates several processes that could impact kidney disease progression, including epithelial cell differentiation and inflammatory cytokine induction.
Jiafa Ren   +9 more
doaj   +1 more source

Identification of novel podocyte stress-response mechanisms in vitro

open access: yes, 2019
Although podocyte injury has been correlated with glomerular disease progression, the mechanisms underlying podocyte response to stress in vivo remain poorly understood.
Haley, Kathryn Elizabeth
core   +1 more source

SPARC Drives Podocyte Mitochondrial Damage and Ferroptosis in Diabetic Kidney Disease Following Klotho Deficiency

open access: yesAdvanced Science, EarlyView.
Klotho deficiency promotes podocyte mitochondrial dysfunction and ferroptosis through activation of the PKCα/CUX1/SPARC/TGFβ‐RII axis. SPARC emerges as a key mediator linking Klotho loss to podocyte injury in DKD and other kidney injury models, suggesting broader implications for CKD progression.
Qing Yang   +11 more
wiley   +1 more source

A comprehensive insight into autophagy and its potential signaling pathways as a therapeutic target in podocyte injury [PDF]

open access: yes, 2022
As part of the glomerular filtration membrane, podocyte is terminally differentiated, structurally unique, and highly specialized in maintaining kidney function.
Lim, Soo Kun   +2 more
core   +3 more sources

Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3‐Dependent Podocyte‐Mesenchymal Transition

open access: yesAdvanced Science, 2023
Podocyte injury plays a critical role in the progression of focal segmental glomerulosclerosis (FSGS). Here, it is reported that B‐cell translocation gene 2 (Btg2) promotes Adriamycin (ADR)‐induced FSGS via Smad3‐dependent podocyte‐mesenchymal transition.
Qiong‐ Dan Hu   +9 more
doaj   +1 more source

Histone deacetylase 9 exacerbates podocyte injury in hyperhomocysteinemia through epigenetic repression of Klotho

open access: yesPharmacological Research, 2023
Although hyperhomocysteinemia (hHcys) has been recognized as an important independent risk factor in the progression of end-stage renal disease and the development of cardiovascular complications related to end-stage renal disease, the mechanisms ...
Min Liu   +14 more
doaj   +1 more source

Mechanisms of Podocyte Injury in Diabetes [PDF]

open access: yesDiabetes, 2009
OBJECTIVE We investigated the role of cytochrome P450 of the 4A family (CYP4A), its metabolites, and NADPH oxidases both in reactive oxygen species (ROS) production and apoptosis of podocytes exposed to high glucose and in OVE26 mice, a model of type 1 diabetes ...
Eid, Assaad A.   +6 more
openaire   +2 more sources

Hepatocyte growth factor signaling ameliorates podocyte injury and proteinuria [PDF]

open access: yes, 2010
Hepatocyte growth factor (HGF) is a potent antifibrotic protein that inhibits kidney fibrosis through several mechanisms. To study its role in podocyte homeostasis, injury, and repair in vivo, we generated conditional knockout mice in which the HGF ...
Liu, Y   +10 more
core   +1 more source

Klotho‐Derived Peptide 1 Protects against Acute Kidney Injury by Directly Targeting Mitochondrial ATAD3A

open access: yesAdvanced Science, EarlyView.
This study uncovers that KP1, a Klotho‐derived peptide, protects the kidney against acute kidney injury, a clinical syndrome with high morbidity and mortality. KP1 enters tubular epithelial cells via endocytosis, directly interacts with the mitochondrial ATAD3A/HIGD2A complex, thereby preventing cytochrome c release, and caspases activation, and ...
Xiaoyao Zhang   +6 more
wiley   +1 more source

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