ArticleCell death & disease2025
Tubular CD44 plays a key role in aggravating AKI through NF-κB p65-mediated mitochondrial dysfunction.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Biomimetic membrane-coated metal nanoplatforms for enhanced BBB penetration and targeted glioblastoma therapy.International journal of pharmaceutics: X · 2026Review
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Unveiling the mechanism of metabolites derived from gut microbiota in the treatment of acute kidney injury via network pharmacology and bioinformatics.Bioresources and bioprocessing · 2026Article
- From matrix to nucleus: CD44 as a central regulator of inflammaging, autophagy, and tissue homeostasis.Biogerontology · 2026Review
- Harmonizing Rigidity and Flexibility: Embedding COF Quantum Dots Into Extracellular Matrix Gel as Carbon Monoxide Depot for Acoustically Triggered Time-Programmable Anti-Infective Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Anti-obesity mechanisms of adzuki bean saponin: a multi-omics and experimental study.NPJ science of food · 2026Article
- Activation of PPARγ Attenuates Age-Related Lacrimal Gland Dysfunction by Alleviating Endoplasmic Reticulum Stress-Mediated Ferroptosis.Investigative ophthalmology & visual science · 2026Article
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- Pi4ka downregulation triggers Creb3l2-dependent lysosomal dysfunction to promote maladaptive tubular remodeling and immune activation in acute kidney injury.Cell death & disease · 2026Article
- NF-κB-driven lymphangiogenesis affects kidney function via a VEGFR-3-mediated pathway.JCI insight · 2026Article
- PGC-1α protects against MASH via Tim23-dependent inhibition of DRP1-mediated ferroptosis.Cell death & disease · 2026Article
- Identification and validation of a novel ferroptosis-related gene signature associated with inherited retinal degeneration in Rd10 mice.Scientific reports · 2026Article
- Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics.Biomedicines · 2026Review
- Mitochondrial dysfunction in sepsis-associated acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Targeting Kupffer Cell CD44-Mediated Ammonia Death via the ELAVL1-GLS Metabolic Circuit in Radiation-Induced Liver Disease.International journal of biological sciences · 2026Article
- Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity.Frontiers in physiology · 2026Review
- Mechanisms of salvianolic acids in kidney disease therapy: advances and perspectives.Frontiers in pharmacology · 2026Review
- Secretory Leukocyte Protease Inhibitor: A Pleiotropic Molecule for the Potential Diagnosis of and Therapy for Acute Kidney Injury.International journal of molecular sciences · 2025Review
- Intracellular Calcium Dysregulation: The Hidden Culprit in the Diabetes-Gout Nexus.Biomedicines · 2025Review
- Emerging applications of nanotechnology in the treatment of acute kidney injury.Nanomedicine (London, England) · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Acute kidney injury (AKI) is in rapid prevalence nowadays. Of note, the underlying mechanisms have not been clarified. Several reports showed a cluster of differentiation-44 (CD44), a cell-surface glycoprotein, might be involved in AKI. However, its role in AKI has not been clearly clarified. Herein, we found CD44 increased in renal tubules in AKI mice. Gene ablation of CD44 improved mitochondrial biogenesis and fatty acid oxidation (FAO) function, further protecting against tubular cell death and kidney injury. Conversely, ectopic CD44 impaired mitochondrial homeostasis and exacerbated tubular cell apoptosis to aggravate AKI progression. From transcriptome sequencing, we found that CD44 induces mitogen-activated protein kinase (MAPK) and NF-κB p65 signaling. Lipidomics also showed that CD44 interfered with multiple aspects of lipid metabolism. We deeply investigated NF-κB p65 inhibited the transcription of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), resulting in mitochondrial dysfunction and cell apoptosis. CD44 also facilitated iron intake to assist cell ferroptosis. Hence, our study provided a new mechanism for AKI, and demonstrated that targeted inhibition on CD44 could be a promising therapeutic strategy to resist AKI.
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