Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases
<p>Cellular functions regulated by lysosomes including autophagy, MVB degradation, lysosomal secretion, phagocytosis, inflammasome activation, membrane repair, and apoptosis. AP, autophagosome; MVB, multivesicular body.</p> "> Figure 2
<p>Regulation of mTORC1 in podocytes. During starvation, inactive mTORC1 has no effects on lysosome function and autophagic flux in podocytes. During diabetic nephropathy (DN), hyperglycemia upregulates TCTP, GLUT3, and C1-Ten, leading to overactivation of mTORC1 and inhibition of autophagy. As a specific mTORC1 inhibitor, rapamycin can prevent lysosome dysfunction, autophagic deficiency, and podocyte injury during diabetes. Reactive oxygen species (ROS) produced by mitochondria has also been reported to prevent mTORC1 activation in podocytes during diabetes.</p> "> Figure 3
<p>Mechanism of inflammatory exosome release in podocytes. It has been reported that in podocytes, pathological stimuli may induce inflammasome activation and lysosome dysfunction. Activated inflammasome produces proinflammatory cytokines, such as IL-1β and IL-18. Lysosome dysfunction leads to reduced MVB degradation and increased exosome release. The proinflammatory cytokines in podocytes may be released through exosome release. The released inflammatory exosomes may induce direct injury of podocytes and inflammatory response, leading to the development of glomerular sclerosis. NLRP3, nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3; ASC, adaptor molecule apoptosis-associated speck-like protein containing a caspase recruitment domain; IL-1β, interleukin-1β; GBM, glomerular basement membrane; EC, endothelial cell.</p> "> Figure 4
<p>Regulation of lysosome trafficking by sphingolipids in podocytes. Dynein-mediated retrograde transport of lysosomes promotes their fusion with MVB. This transport is dependent on the TRPML1 channel-mediated Ca<sup>2+</sup> release. In the lysosome, ASM converts SM into CER and AC converts CER to Sph. These sphingolipids, SM, Cer, and Sph had different effects on TRPML1 channel activity in podocytes, with inhibition by SM, no effect from Cer, but enhancement by Sph. SM, sphingomyelin; Cer; ceramide; Sph, sphingosine.</p> ">
Abstract
:1. Introduction
2. Different Types of Lysosomes
3. Cellular Functions Regulated by Lysosomes
3.1. Autophagic Flux
3.2. Lipid Metabolism
3.3. Inflammasome Activation
3.4. Exosome Release
4. Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases
4.1. Diabetic Nephropathy
4.2. Glomerular Injury during Fabry Disease
4.3. Hyperhomocysteinemic Nephropathy
4.4. Obesity-Induced Podocyte Injury and Glomerular Disease
4.5. APOL1-Associated Nephropathy
5. Therapeutic Potential of Chronic Glomerular Diseases by Restoring Lysosome Function
6. Concluding Remarks
Funding
Conflicts of Interest
References
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Li, G.; Kidd, J.; Li, P.-L. Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases. Int. J. Mol. Sci. 2020, 21, 1559. https://doi.org/10.3390/ijms21051559
Li G, Kidd J, Li P-L. Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases. International Journal of Molecular Sciences. 2020; 21(5):1559. https://doi.org/10.3390/ijms21051559
Chicago/Turabian StyleLi, Guangbi, Jason Kidd, and Pin-Lan Li. 2020. "Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases" International Journal of Molecular Sciences 21, no. 5: 1559. https://doi.org/10.3390/ijms21051559