Controversies in Podocyte Loss: Death or Detachment?

Yin, Liu; Lu, Yu; He, John Cijiang; Chen, Anqun

doi:10.3389/fcell.2021.771931

Cited by 30 publications

(28 citation statements)

References 80 publications

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“…This would be consistent with the clinical observation that in progressive glomerular diseases, injured podocytes are lost from the glomerular capillary tuft, into the urinary space. 21 …”

Section: Resultsmentioning

confidence: 99%

Transcriptomic Analysis of Human Podocytes In Vitro: Effects of Differentiation and APOL1 Genotype

Yoshida

Latt²,

Rosenberg³

et al. 2023

Kidney International Reports

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“…This would be consistent with the clinical observation that in progressive glomerular diseases, injured podocytes are lost from the glomerular capillary tuft, into the urinary space. 21 …”

Section: Resultsmentioning

confidence: 99%

Transcriptomic Analysis of Human Podocytes In Vitro: Effects of Differentiation and APOL1 Genotype

Yoshida

Latt²,

Rosenberg³

et al. 2023

Kidney International Reports

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“…Apoptosis of podocytes has been demonstrated in cell culture studies using various conventional techniques, while apoptosis in vivo has been reported in rodent models, mainly based on tissue staining with terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) or caspase-3 staining. Interestingly, apoptosis has not been observed in human podocytes by electron microscopy (Kriz et al, 2013;Nagata, 2016;Yin et al, 2021). These discrepant results between rodents and humans may be in part related to experimental techniques, or may represent species differences.…”

Section: The Podocyte In Health and Diseasementioning

confidence: 99%

The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond

Navarro-Betancourt

Cybulsky

2022

Front. Mol. Med

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Endoplasmic reticulum (ER) function is vital for protein homeostasis (“proteostasis”). Protein misfolding in the ER of podocytes (glomerular visceral epithelial cells) is an important contributor to the pathogenesis of human glomerular diseases. ER protein misfolding causes ER stress and activates a compensatory signaling network called the unfolded protein response (UPR). Disruption of the UPR, in particular deletion of the UPR transducer, inositol-requiring enzyme 1α (IRE1α) in mouse podocytes leads to podocyte injury and albuminuria in aging, and exacerbates injury in glomerulonephritis. The UPR may interact in a coordinated manner with autophagy to relieve protein misfolding and its consequences. Recent studies have identified novel downstream targets of IRE1α, which provide new mechanistic insights into proteostatic pathways. Novel pathways of IRE1α signaling involve reticulophagy, mitochondria, metabolism, vesicular trafficking, microRNAs, and others. Mechanism-based therapies for glomerulopathies are limited, and development of non-invasive ER stress biomarkers, as well as targeting ER stress with pharmacological compounds may represent a therapeutic opportunity for preventing or attenuating progression of chronic kidney disease.

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“…Indeed, impaired autophagy causes podocyte loss [ 125 ]. For instance, deleting Atg5 gene in podocytes leads to glomerular lesions that are concomitant with podocyte loss and albuminuria [ 126 ].…”

Section: Autophagy In Diabetic Nephropathymentioning

confidence: 99%

Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis

Erekat

2022

Med Sci Monit

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Diabetic nephropathy is a common complication of type I and type II diabetes, in which renal glomeruli are destroyed, resulting in renal damage, proteinuria, and hypertension. Apoptosis, autophagy, and necroptosis are 3 forms of programmed cell death that have been implicated in the pathogenesis of diabetic nephropathy. Apoptosis of podocytes leads to glomerular injury and podocyte depletion, which are associated with proteinuria and glomerular structural damage in diabetic nephropathy. Additionally, epithelial cells in the proximal convoluted tubules also undergo apoptosis in diabetic nephropathy, leading to tubular atrophy, which causes tubular cell depletion and the subsequent formation of atubular glomeruli in association with the loss of renal function. On the other hand, insufficiency of autophagy has been correlated with the pathogenesis of diabetic nephropathy. For instance, decreased autophagic activity has been shown in podocytes of the diabetic kidney, causing variations in podocyte function and subsequent disruption to the glomerular filtration barrier. Furthermore, attenuated autophagic activity has also been demonstrated in proximal tubular cells of the diabetic kidney, resulting in the buildup of impaired molecules and organelles, which are normally broken down by autophagy, leading to proteinuria. Moreover, necroptosis might have a key role in podocyte damage and subsequent decline in diabetic nephropathy. Thus, this article aims to review the mechanisms and effects of programmed cell death in diabetic nephropathy, including the roles of apoptosis, autophagy, and necroptosis.

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Controversies in Podocyte Loss: Death or Detachment?

Cited by 30 publications

References 80 publications

Transcriptomic Analysis of Human Podocytes In Vitro: Effects of Differentiation and APOL1 Genotype

Transcriptomic Analysis of Human Podocytes In Vitro: Effects of Differentiation and APOL1 Genotype

The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond

Programmed Cell Death in Diabetic Nephropathy: A Review of Apoptosis, Autophagy, and Necroptosis

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