ArticleMedical science monitor basic research2020
Paclitaxel Ameliorates Palmitate-Induced Injury in Mouse Podocytes.
Article in Medical science monitor basic research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Targeting endoplasmic reticulum stress: an innovative therapeutic strategy for podocyte-related kidney diseases.Journal of translational medicine · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.Experimental & molecular medicine · 2024Article
- Natural products derived from traditional Chinese medicines targeting ER stress for the treatment of kidney diseases.Renal failure · 2024Review
- Natural compounds improve diabetic nephropathy by regulating the TLR4 signaling pathway.Journal of pharmaceutical analysis · 2024Review
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Effects of cytokine signaling inhibition on inflammation-driven tissue remodeling.Current research in pharmacology and drug discovery · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Palmitate, a common saturated free fatty acid, is increased in patients with diabetic nephropathy (DN). Excessive palmitate in kidney is known to cause proteinuria and fibrosis. Several studies have demonstrated that paclitaxel has anti-fibrotic and anti-inflammatory effects on kidney disease. However, whether paclitaxel can relieve podocyte injury is unclear. MATERIAL AND METHODS Immortalized mouse podocytes were used as an in vitro system. Palmitate was used to induce podocyte injury. Podocytes were divided into 4 groups: bovine serum albumin, palmitate, palmitate+1 nM paclitaxel, and palmitate+5 nM paclitaxel. The effects of paclitaxel on palmitate-induced podocyte injury were analyzed by western blot and real-time PCR. Intracellular reactive oxygen species (ROS) generation and podocyte cytoskeletons were analyzed using CM-H2DCF-DA and phalloidin staining. RESULTS Paclitaxel restored downregulated expression of nephrin and synaptopodin and upregulated VEGF expression after injury induced by palmitate. Remarkably, palmitate-induced actin cytoskeleton rearrangement in podocytes was repaired by paclitaxel. Four endoplasmic reticulum stress markers, ATF-6alpha, Bip, CHOP, and spliced xBP1, were significantly increased in palmitate-treated podocytes compared with control podocytes. Such increases were decreased by paclitaxel treatment. Palmitate-induced ROS generation was ameliorated by paclitaxel. Elevated Nox4 expression was also improved by paclitaxel. Paclitaxel alleviated the expression levels of the antioxidant molecules, Nrf-2, HO-1, SOD-1, and SOD-2. The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3. Furthermore, paclitaxel suppressed the palmitate-induced fibrosis molecules, fibronectin and TGF-ß1. CONCLUSIONS This study suggests that paclitaxel could be a therapeutic agent for treating palmitate-induced podocyte injury in DN.
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