ArticleDrug design, development and therapy2025
Cytoskeleton Rearrangement Decreases Mitochondrial Fatty Acid Oxidation in Renal Tubular Epithelial Cells Contributing to Renal Fibrogenesis.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The epithelial-mesenchymal transition (EMT) plays an important role in renal fibrosis. Defective fatty acid oxidation (FAO) is the metabolic hallmark in injured tubular epithelial cells (TECs) contributing to renal fibrogenesis. Dysregulated cytoskeleton is believed to be an important element of renal injury and its function has been linked to cell metabolism, but little is known about the influence of the cytoskeleton on FAO in TECs. Herein, we aimed to investigate the protective effects and molecular mechanisms of pharmacological stabilization of the cytoskeleton against unilateral ureteric obstruction (UUO) -induced renal tubulointerstitial fibrosis. Materials and Methods: TGF-β1-treated primary tubular epithelial cells (PTECs) and UUO mice served as renal interstitial fibrosis (RIF) models, with or without pharmacological cytoskeleton stabilization by Bis-T-23 (TargetMol, T30479; 20 mg/kg/day intraperitoneally in vivo; 5 μM in vitro). Biomarkers, HE staining, PAS staining, Masson staining, Sirius red staining, and TUNEL assay were used to assess kidney function and apoptosis. Real-time quantitative PCR (qPCR), Western blotting and immunohistochemistry (IHC) were performed to measure mRNA and protein expression levels respectively. PTECs viability was assessed by CCK-8 assay. Bulk mRNA sequencing was used for transcriptomic analysis of cellular metabolism. FITC-phalloidin fluorescence staining was used to detect the cytoskeleton. Fluorescent co-staining was used to detect the interactions between lipid droplets (LDs) and mitochondria. Results: Pharmacological stabilization of the cytoskeleton alleviated tubulointerstitial injury, functional changes and TEC damage in UUO mouse models. Stabilization of cytoskeleton restored FAO and enhanced FAO-associated respiration impaired by UUO injury. Here, we demonstrate that cytoskeleton rearrangement is a critical regulator of mitochondrial FAO in TECs both in vitro and in vivo. We further show that this cytoskeleton-dependent regulation of FAO occurs through altered interactions between LDs and mitochondria. Conclusion: These findings indicate that cytoskeleton stabilization is required to maintain TECs metabolism and that therapeutic manipulation of cytoskeleton remodeling could protect the kidney from fibrogenesis conditions.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.