HIVAN associated tubular pathology with reference to ER stress, mitochondrial changes, and autophagy

Katuri, Akhil; Bryant, Joseph; Patel, Dhruvil; Patel, Vivek P.; Andhavarapu, Sanketh; Asemu, Girma; Davis, Harry; Makar, Tapas K.

doi:10.1016/j.yexmp.2018.12.009

Cited by 10 publications

(4 citation statements)

References 66 publications

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“…22 Recent reports have identified several injury pathways, including NLRP3 23 and mitochondrial dysfunction. 24,25 Bulk multi-omics approaches using mRNA microarrays and protein-DNA arrays 26 identified homeo-domain interacting protein kinase-2 (HIPK2) as a regulator of Tg26 renal pathology; this was confirmed in recent reports. 27, 28 A mRNA microarray approach characterized bulk transcriptional profiles during progressive renal disease.…”

Section: Introductionmentioning

confidence: 80%

PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy

Yoshida

Latt

Rosenberg

et al. 2022

Preprint

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HIV remains prevalent in the USA and chronic kidney disease remains a major cause of morbidity in HIV-1-positive patients. Host double-stranded RNA (dsRNA)-activated protein kinase (PKR) is a sensor for viral dsRNA, including HIV-1. We show that PKR inhibition by compound C16 ameliorates the HIV-associated nephropathy (HIVAN) kidney phenotype in the Tg26 transgenic mouse model, with reversal of mitochondrial dysfunction. Combined analysis of single-nucleus RNA-seq and bulk RNA-seq data revealed that oxidative phosphorylation was one of the most downregulated pathways and identified Stat3 as a potential mediating factor. We identified in Tg26 mice a novel proximal tubular cell cluster enriched in mitochondrial transcripts. Podocytes showed high HIV-1 gene expression and dysregulation of cytoskeleton-related genes and these cells dedifferentiated and were lost. Cell-cell interaction analysis suggested that the profibrogenic PKR-STAT3-PDGF-D pathway was activated in injured proximal tubules and was triggered by PDGFRB-expressing fibroblasts throughout the cortex. These findings suggest that PKR inhibition and mitochondrial rescue as potential novel therapeutic approaches for HIVAN.

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Section: Introductionmentioning

confidence: 80%

PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy

Yoshida

Latt

Rosenberg

et al. 2022

Preprint

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“…Further studies revealed that APOL1 RRVs induced an autophagy blockade in podocytes by multiple mechanisms [ 83 , 89 , 90 ], as listed in Table 2 .…”

Section: Human Immunodeficiency Virus (Hiv) and Glomerulonephritismentioning

confidence: 99%

The Human Virome and Its Crosslink with Glomerulonephritis and IgA Nephropathy

Sallustio

Picerno

Montenegro

et al. 2023

IJMS

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The prokaryotic, viral, fungal, and parasitic microbiome exists in a highly intricate connection with the human host. In addition to eukaryotic viruses, due to the existence of various host bacteria, phages are widely spread throughout the human body. However, it is now evident that some viral community states, as opposed to others, are indicative of health and might be linked to undesirable outcomes for the human host. Members of the virome may collaborate with the human host to retain mutualistic functions in preserving human health. Evolutionary theories contend that a particular microbe’s ubiquitous existence may signify a successful partnership with the host. In this Review, we present a survey of the field’s work on the human virome and highlight the role of viruses in health and disease and the relationship of the virobiota with immune system control. Moreover, we will analyze virus involvement in glomerulonephritis and in IgA nephropathy, theorizing the molecular mechanisms that may be responsible for the crosslink with these renal diseases.

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“…Renal tubular epithelial cell co-cultured with infected T cells becomes susceptible to HIV. HIV DNA and RNA were detected in renal tubular epithelial cells by in situ hybridization of biopsies collected from patients with HIV-associated nephropathy ( Katuri et al., 2019 ). In addition, it has been reported that integrated HIV DNA can be detected after in vitro infection of liver cell lines and primary liver cells, and the release of infectious viruses was also found in the liver epithelium ( Ganesan et al., 2018 ).…”

Section: The Cell Reservoir Of Hivmentioning

confidence: 99%

The reservoir of latent HIV

Chen

Zhou

Zhang

et al. 2022

Front. Cell. Infect. Microbiol.

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The persistence of latent reservoir of the human immunodeficiency virus (HIV) is currently the major challenge in curing HIV infection. After HIV infects the human body, the latent HIV is unable to be recognized by the body’s immune system. Currently, the widely adopted antiretroviral therapy (ART) is also unble to eliminate it, thus hindering the progress of HIV treatment. This review discusses the existence of latent HIV vault for HIV treatment, its formation and factors affecting its formation, cell, and tissue localization, methods for detection and removing latent reservoir, to provide a comprehensive understanding of latent HIV vault, in order to assist in the future research and play a potential role in achieving HIV treatment.

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HIVAN associated tubular pathology with reference to ER stress, mitochondrial changes, and autophagy

Cited by 10 publications

References 66 publications

PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy

PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy

The Human Virome and Its Crosslink with Glomerulonephritis and IgA Nephropathy

The reservoir of latent HIV

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