ArticleKidney international2021
Kidney epithelial targeted mitochondrial transcription factor A deficiency results in progressive mitochondrial depletion associated with severe cystic disease.
Article in Kidney international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- The Role of Mitochondria in Polycystic Kidney Disease.International journal of molecular sciences · 2026Review
- PAX gene expression in autosomal dominant polycystic kidney disease contributes to cyst expansion and regulates a gene network associated with cyst growth.Human molecular genetics · 2026Article
- Regional metabolic analysis of structurally preserved kidney slices by ex vivo respirometry.American journal of physiology. Renal physiology · 2025Article
- Mitochondrial organization in the developing proximal tubule is controlled by LRRK2.Nature communications · 2025Article
- Guanine quadruplexes mediate mitochondrial RNA polymerase pausing.BMC biology · 2025Article
- GLIS3: A novel transcriptional regulator of mitochondrial functions and metabolic reprogramming in postnatal kidney and polycystic kidney disease.Molecular metabolism · 2024Article
- Article
- The key role of altered tubule cell lipid metabolism in kidney disease development.Kidney international · 2024Review
- FGF21 and autophagy coordinately counteract kidney disease progression during aging and obesity.Autophagy · 2024Article
- Correction to: YY1 inactivated transcription co-regulator PGC-1α to promote mitochondrial dysfunction of early diabetic nephropathy-associated tubulointerstitial fibrosis.Cell biology and toxicology · 2023Article
- Regulation of PGC-1α of the Mitochondrial Energy Metabolism Pathway in the Gills of Indian Medaka (International journal of molecular sciences · 2023Article
- The impact of metabolic stressors on mitochondrial homeostasis in a renal epithelial cell model of methylmalonic aciduria.Scientific reports · 2023Article
- YY1 inactivated transcription co-regulator PGC-1α to promote mitochondrial dysfunction of early diabetic nephropathy-associated tubulointerstitial fibrosis.Cell biology and toxicology · 2023Article
- SIX4 upregulates IDH1 and metabolic reprogramming to promote osteosarcoma progression.Journal of cellular and molecular medicine · 2023Article
- Gene Editing Technologies Targeting TFAM and Its Relation to Mitochondrial Diseases.Advances in experimental medicine and biology · 2023Article
- Intact mitochondrial substrate efflux is essential for prevention of tubular injury in a sex-dependent manner.JCI insight · 2022Article
- Dopamine D2 Receptor Signaling Attenuates Acinar Cell Necroptosis in Acute Pancreatitis through the Cathepsin B/TFAM/ROS Pathway.Oxidative medicine and cellular longevity · 2022Article
- MORG1-A Negative Modulator of Renal Lipid Metabolism in Murine Diabetes.Biomedicines · 2021Article
- Mitochondrial DNA-Mediated Inflammation in Acute Kidney Injury and Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2021Review
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Abnormal mitochondrial function is a well-recognized feature of acute and chronic kidney diseases. To gain insight into the role of mitochondria in kidney homeostasis and pathogenesis, we targeted mitochondrial transcription factor A (TFAM), a protein required for mitochondrial DNA replication and transcription that plays a critical part in the maintenance of mitochondrial mass and function. To examine the consequences of disrupted mitochondrial function in kidney epithelial cells, we inactivated TFAM in sine oculis-related homeobox 2-expressing kidney progenitor cells. TFAM deficiency resulted in significantly decreased mitochondrial gene expression, mitochondrial depletion, inhibition of nephron maturation and the development of severe postnatal cystic disease, which resulted in premature death. This was associated with abnormal mitochondrial morphology, a reduction in oxygen consumption and increased glycolytic flux. Furthermore, we found that TFAM expression was reduced in murine and human polycystic kidneys, which was accompanied by mitochondrial depletion. Thus, our data suggest that dysregulation of TFAM expression and mitochondrial depletion are molecular features of kidney cystic disease that may contribute to its pathogenesis.
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