Daniela Nieri
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Daniela Nieri has a total of 26 co-authors. Here are the top co-authors by number of shared publications:
Adia M. Ouellette
Department of Chemistry and Biochemistry, University of Moncton
1 shared publication- Alaa Othman
ETH Zurich
1 shared publication - Alessandro Luciani
Institute of Physiology, Mechanisms of Inherited Kidney Diseases Group, University of Zurich, Zurich, Switzerland
1 shared publication - Alina Sergeevna Ustiugova
Insilico Medicine AI Limited, Abu Dhabi, UAE
1 shared publication Andrea Raimondi
Institute for Research in Biomedicine, Italian Swiss University
1 shared publication- Andrew Schaefer
Mitochondrial Research Group, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University
1 shared publication
Latest Publications
- Open Access
Autophagy regulator ATG7 links lipid metabolism to cell-fate decisions in kidney tubule health and disease
Homeostasis in the kidney proximal tubule (PT) requires coordination between metabolism and differentiation, yet the mechanisms governing this balance remain elusive. Here, we integrate model organisms, multiomics profiling, and human genetics to identify the autophagy regulator ATG7 as a key determinant of cell-fate decisions, sustaining PT specialization in health and contributing to dysfunction in disease. In mice, PT-specific deletion of ATG7 reprograms differentiated cells into anabolic, proliferative states, impairing their specialized function and causing kidney tubulopathy. Mechanistically, loss of ATG7-dependent autophagy hinders lipid droplet clearance and restricts fatty-acid oxidation (FAO), leading to energy depletion and functional decline. In zebrafish pronephros, re-expression of wild-type ATG7 restores homeostasis in atg7 mutants, while pharmacological FAO inhibition triggers dysfunction. In humans, ATG7 variants associate with cardio-renal-metabolic traits and increased disease risk, whereas low ATG7 expression correlates with transcriptional signatures of metabolic reprogramming, loss of epithelial markers, and poor prognosis in renal cell carcinoma. These findings establish a conserved genetic paradigm that links autophagy to kidney epithelial cell-fate specialization, with implications for disease, cancer, and metabolic health.
Open AccessAutophagy regulator ATG7 links lipid metabolism to cell-fate decisions in kidney tubule health and disease
Homeostasis in the kidney proximal tubule (PT) requires coordination between metabolism and differentiation, yet the mechanisms governing this balance remain elusive. Here, we integrate model organisms, multiomics profiling, and human genetics to identify the autophagy regulator ATG7 as a key determinant of cell-fate decisions, sustaining PT specialization in health and contributing to dysfunction in disease. In mice, PT-specific deletion of ATG7 reprograms differentiated cells into anabolic, proliferative states, impairing their specialized function and causing kidney tubulopathy. Mechanistically, loss of ATG7-dependent autophagy hinders lipid droplet clearance and restricts fatty-acid oxidation (FAO), leading to energy depletion and functional decline. In zebrafish pronephros, re-expression of wild-type ATG7 restores homeostasis in atg7 mutants, while pharmacological FAO inhibition triggers dysfunction. In humans, ATG7 variants associate with cardio-renal-metabolic traits and increased disease risk, whereas low ATG7 expression correlates with transcriptional signatures of metabolic reprogramming, loss of epithelial markers, and poor prognosis in renal cell carcinoma. These findings establish a conserved genetic paradigm that links autophagy to kidney epithelial cell-fate specialization, with implications for disease, cancer, and metabolic health.