ArticleAutophagy2025
AMPK protects proximal tubular epithelial cells from lysosomal dysfunction and dedifferentiation induced by lipotoxicity.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Human adipose-derived mesenchymal stem cells ameliorate Diabetic Kidney Disease by restoring macrophage efferocytosis.Stem cell research & therapy · 2026Article
- Identification of ATF3 as a Potential Key Biomarker for Hypertensive Nephropathy via Single-Cell Transcriptome Sequencing.Inflammation · 2026Article
- Carnitine dysregulation in diabetic kidney disease: from pathogenic mechanism to precision biomarker.Journal of translational medicine · 2026Review
- Effects of NAD⁺ repletion with Nicotinamide riboside on obesity-induced chronic kidney disease and renal cell lipotoxicity.Scientific reports · 2026Article
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Heterogeneity in lysosomal dynamics and metabolic functions along the kidney proximal tubule.Nature communications · 2026Article
- Review
- Exercise Improves Sarcopenic Obesity Through Inhibition of Ferroptosis and Activation of the AMPK/ACC Pathway.International journal of molecular sciences · 2026Article
- Lysosomal checkpoints in renal autoimmunity: from antigen processing to metabolic-immune crosstalk.Frontiers in immunology · 2026Review
- Autophagy in kidney physiology: from cellular quality control to organ metabolism.Autophagy reports · 2026Review
- A Lipid Road to Neuroimmunology: Fatty Acids Linking Immune and Nervous Systems.Neuroimmunomodulation · 2026Review
- The endo-lysosomal-lipid axis: bidirectional interactions between membrane trafficking dysfunction and lipid metabolic disorders.Frontiers in cell and developmental biology · 2026Review
- IGFBP7: A potential target for tubular lipogenesis in CKD.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Renal proximal tubules are a primary site of injury in metabolic diseases. In obese patients and animal models, proximal tubular epithelial cells (PTECs) display dysregulated lipid metabolism, organelle dysfunctions, and oxidative stress that contribute to interstitial inflammation, fibrosis and ultimately end-stage renal failure. Our research group previously pointed out AMP-activated protein kinase (AMPK) decline as a driver of obesity-induced renal disease. Because PTECs display high macroautophagic/autophagic activity and rely heavily on their endo-lysosomal system, we investigated the effect of lipid stress on autophagic flux and lysosomes in these cells. Using a model of highly differentiated primary PTECs challenged with palmitate, our data placed lysosomes at the cornerstone of the lipotoxic phenotype. As soon as 6 h after palmitate exposure, cells displayed impaired lysosomal acidification subsequently leading to autophagosome accumulation and activation of lysosomal biogenesis. We also showed the inability of lysosomal quality control to restore acidic pH which finally drove PTECs dedifferentiation. When palmitate-induced AMPK activity decline was prevented by AMPK activators, lysosomal acidification and the differentiation profile of PTECs were preserved. Our work provided key insights on the importance of lysosomes in PTECs homeostasis and lipotoxicity and demonstrated the potential of AMPK in protecting the organelle from lipid stress.
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Registered trials
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