ArticleProceedings of the National Academy of Sciences of the United States of America2018
Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 66 citations in OpenAlex.
- Force-modulated structural landscape of the catch bonding F-actin crosslinker α-actinin-4.bioRxiv : the preprint server for biology · 2026Article
- Cellular mechanisms of traumatic brain injury.npj biological physics and mechanics · 2025Review
- Synthetic, multi-dynamic hydrogels by uniting stress-stiffening and supramolecular polymers.Science advances · 2024Article
- Identification of Pathogenic Pathways for Recurrence of Focal Segmental Glomerulosclerosis after Kidney Transplantation.Diagnostics (Basel, Switzerland) · 2024Article
- From stress fiber to focal adhesion: a role of actin crosslinkers in force transmission.Frontiers in cell and developmental biology · 2024Review
- Actin crosslinking by α-actinin averts viscous dissipation of myosin force transmission in stress fibers.iScience · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Placental proteome in late‑onset of fetal growth restriction.Molecular medicine reports · 2022Article
- WDR73 Depletion Destabilizes PIP4K2C Activity and Impairs Focal Adhesion Formation in Galloway-Mowat Syndrome.Biology · 2022Article
- ANGPTL3 is involved in kidney injury in high-fat diet-fed mice by suppressing ACTN4 expression.Lipids in health and disease · 2022Article
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2021Review
- Review
- UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021Review
- Cytoskeleton Rearrangements Modulate TRPC6 Channel Activity in Podocytes.International journal of molecular sciences · 2021Article
- Expression correlation attenuates within and between key signaling pathways in chronic kidney disease.BMC medical genomics · 2020Article
- Phosphorylation of key podocyte proteins and the association with proteinuric kidney disease.American journal of physiology. Renal physiology · 2020Review
- Dynamic actin cross-linking governs the cytoplasm's transition to fluid-like behavior.Molecular biology of the cell · 2020Article
- Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.Journal of the American Society of Nephrology : JASN · 2020Article
- Connectivity and plasticity determine collagen network fracture.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Actin modulates shape and mechanics of tubular membranes.Science advances · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
α-Actinin-4 (ACTN4) bundles and cross-links actin filaments to confer mechanical resilience to the reconstituted actin network. How this resilience is built and dynamically regulated in the podocyte, and the cause of its failure in ACTN4 mutation-associated focal segmental glomerulosclerosis (FSGS), remains poorly defined. Using primary podocytes isolated from wild-type (WT) and FSGS-causing point mutant Actn4 knockin mice, we report responses to periodic stretch. While WT cells largely maintained their F-actin cytoskeleton and contraction, mutant cells developed extensive and irrecoverable reductions in these same properties. This difference was attributable to both actin material changes and a more spatially correlated intracellular stress in mutant cells. When stretched cells were further challenged using a cell adhesion assay, mutant cells were more likely to detach. Together, these data suggest a mechanism for mutant podocyte dysfunction and loss in FSGS-it is a direct consequence of mechanical responses of a cytoskeleton that is brittle.
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