ArticleLaboratory investigation; a journal of technical methods and pathology2021
Nuclear exclusion of YAP exacerbates podocyte apoptosis and disease progression in Adriamycin-induced focal segmental glomerulosclerosis.
Article in Laboratory investigation; a journal of technical methods and pathology, 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, 34 citations in OpenAlex.
- GADD45A may be a potential biomarker associated with endoplasmic reticulum stress in focal segmental glomerulosclerosis.Biochemistry and biophysics reports · 2026Article
- FGFR1/YAP1 signaling in endothelial cells drives renal fibrosis and offers a therapeutic target.Frontiers in pharmacology · 2026Article
- Podocyte YAP and TAZ hyperactivation drives glomerular epithelial proliferative diseases in mice and humans.Science translational medicine · 2025Article
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Refining the adriamycin-induced focal segmental glomerulosclerosis mouse model to improve reproducibility and animal welfare.Animal models and experimental medicine · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025Article
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Apoptosis in kidney tissue of senior and geriatric cats with chronic kidney disease.The Journal of veterinary medical science · 2025Article
- The Hippo Pathway in Kidney Development.Encyclopedia · 2025Article
- Novel Pathogenic Mutation of P209L in TRPC6 Gene Causes Adult Focal Segmental Glomerulosclerosis.Biochemical genetics · 2024Article
- YAP1 preserves tubular mitochondrial quality control to mitigate diabetic kidney disease.Redox biology · 2024Article
- Mechanosensitive Differentiation of Human iPS Cell-Derived Podocytes.Bioengineering (Basel, Switzerland) · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Article
- The role of the FSGS disease gene product and nuclear pore protein NUP205 in regulating nuclear localization and activity of transcriptional regulators YAP and TAZ.Human molecular genetics · 2023Article
- Proximal TubularInternational journal of molecular sciences · 2023Article
- Blocking ribosomal protein S6 phosphorylation inhibits podocyte hypertrophy and focal segmental glomerulosclerosis.Kidney international · 2022Article
- hucMSC-sEVs-Derived 14-3-3Oxidative medicine and cellular longevity · 2022Article
- Post-Transplant Recurrence of Focal Segmental Glomerulosclerosis: Circulating Factors, Molecular Biomarkers, and Treatments.Kidney diseases (Basel, Switzerland)Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal segmental glomerulosclerosis (FSGS) is a chronic glomerular disease with poor clinical outcomes. Podocyte loss via apoptosis is one important mechanism underlying the pathogenesis of FSGS. Recently, Yes-associated-protein (YAP), a key downstream protein in the Hippo pathway, was identified as an activator for multiple gene transcriptional factors in the nucleus to control cell proliferation and apoptosis. To investigate the potential role of YAP in the progression of FSGS, we examined kidney samples from patients with minimal change disease or FSGS and found that increases in podocyte apoptosis is positively correlated with the cytoplasmic distribution of YAP in human FSGS. Utilizing an established mT/mG transgenic mouse model and primary cultured podocytes, we found that YAP was distributed uniformly in nucleus and cytoplasm in the podocytes of control animals. Adriamycin treatment induced gradual nuclear exclusion of YAP with enhanced phospho-YAP/YAP ratio, accompanied by the induction of podocyte apoptosis both in vivo and in vitro. Moreover, we used verteporfin to treat an Adriamycin-induced FSGS mouse model, and found YAP inhibition by verteporfin induced nuclear exclusion of YAP, thus increasing podocyte apoptosis and accelerating disease progression. Therefore, our findings suggest that YAP nuclear distribution and activation in podocytes is an important endogenous anti-apoptotic mechanism during the progression of FSGS.
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