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Single-cell analysis highlights differences in druggable pathways underlying adaptive or fibrotic kidney regeneration

ABSTRACT: Single-cell analysis highlights differences in druggable pathways underlying adaptive or fibrotic kidney regeneration

PROVIDER: PRJNA748099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15195000.fastq.gz	Fastqsanger.gz
	SRR15195001.fastq.gz	Fastqsanger.gz
	SRR15195002.fastq.gz	Fastqsanger.gz
	SRR15195003.fastq.gz	Fastqsanger.gz
	SRR15195004.fastq.gz	Fastqsanger.gz

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Single-cell analysis highlights differences in druggable pathways underlying adaptive or fibrotic kidney regeneration

Project description:The kidney tubules have tremendous capacity to repair after acute injury, however, pathways guiding adaptive and maladaptive (fibrotic) repair are poorly understood. We developed a model of adaptive and maladaptive kidney regeneration by titrating ischemic injury dose. We performed detailed biochemical and histological analysis and profiled transcriptomic changes at bulk and single-cell level in >110,000 cells over time. Our analysis highlighted kidney proximal tubule (PT) cells as key susceptible cells to injury. Adaptive PT repair correlated with fatty acid oxidation and oxidative phosphorylation. We identified a specific maladaptive/profibrotic PT cluster after long ischemia. These cells expressed proinflammatory and profibrotic cytokines and myeloid cell chemotactic factor. Druggability analysis highlighted pyroptosis and ferroptosis as vulnerable pathways in these profibrotic cells. Pharmacological targeting of pyroptosis/ferroptosis in animal model, pushed cells towards adaptive repair and successfully reduced fibrosis. In summary, our single-cell analysis defined key differences in adaptive and maladaptive repair and identified druggable pathways for pharmacological intervention to prevent kidney fibrosis.

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Single-cell analysis highlights differences in druggable pathways underlying adaptive or fibrotic kidney regeneration.

Project description:The kidney has tremendous capacity to repair after acute injury, however, pathways guiding adaptive and fibrotic repair are poorly understood. We developed a model of adaptive and fibrotic kidney regeneration by titrating ischemic injury dose. We performed detailed biochemical and histological analysis and profiled transcriptomic changes at bulk and single-cell level (> 110,000 cells) over time. Our analysis highlights kidney proximal tubule cells as key susceptible cells to injury. Adaptive proximal tubule repair correlated with fatty acid oxidation and oxidative phosphorylation. We identify a specific maladaptive/profibrotic proximal tubule cluster after long ischemia, which expresses proinflammatory and profibrotic cytokines and myeloid cell chemotactic factors. Druggability analysis highlights pyroptosis/ferroptosis as vulnerable pathways in these profibrotic cells. Pharmacological targeting of pyroptosis/ferroptosis in vivo pushed cells towards adaptive repair and ameliorates fibrosis. In summary, our single-cell analysis defines key differences in adaptive and fibrotic repair and identifies druggable pathways for pharmacological intervention to prevent kidney fibrosis.

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Project description:In this study, two gene expression analyses were performed. The first analysis, comparing the DEGs between fibrotic and non-fibrotic tissue, revealed genes which may play a role in testicular fibrosis, including VCAM1. In addition, this analysis revealed a pertinent role for genes involved in the TGF-β1 pathway. Secondly, a differential gene expression analysis between KS and TA samples was performed. GO analysis revealed genes involved in the chronic inflammatory responses. When comparing the X-linked genes of the first analysis (fibrotic versus non-fibrotic) with those of the second analysis (KS versus TA), X-linked fibrotic genes involved in KS revealed, i.e. MXRA5, DCX and VCX3B. Their potential role in KS-related testicular fibrosis needs further study.

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