Andrea Curtabbi

ORCID: 0000-0002-5185-4431
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • RNA modifications and cancer
  • Muscle Physiology and Disorders
  • Autophagy in Disease and Therapy
  • Adipose Tissue and Metabolism
  • Epigenetics and DNA Methylation
  • Metabolism and Genetic Disorders
  • Endoplasmic Reticulum Stress and Disease
  • Biochemical and Molecular Research
  • Immune cells in cancer
  • Diet and metabolism studies
  • Immune Cell Function and Interaction
  • Cancer, Hypoxia, and Metabolism
  • Tissue Engineering and Regenerative Medicine
  • Photosynthetic Processes and Mechanisms
  • Adipokines, Inflammation, and Metabolic Diseases
  • Atherosclerosis and Cardiovascular Diseases
  • Cardiac Fibrosis and Remodeling
  • Neonatal Respiratory Health Research

Spanish National Centre for Cardiovascular Research
2022-2025

Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable
2023

Increasing evidence has pointed to the important function of T cells in controlling immune homeostasis and pathogenesis after myocardial infarction (MI), although underlying molecular mechanisms remain elusive. In this study, a broad analysis markers 283 patients revealed significant CD69 overexpression on Tregs MI. Our results mice showed that expression increased survival left anterior descending (LAD) coronary artery ligation. Cd69–/– developed strong IL-17+ γδT cell responses ischemia...

10.1172/jci152418 article EN cc-by Journal of Clinical Investigation 2022-09-06

Obesity poses a global health challenge, demanding deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role mitochondrial protein Methylation-controlled J (MCJ/DnaJC15) in orchestrating brown (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident human mouse samples. MCJKO mice, even without UCP1, fundamental thermogenic protein, exhibit elevated BAT Electron microscopy unveils changes morphology resembling activation....

10.1038/s41467-024-54353-4 article EN cc-by-nc-nd Nature Communications 2025-01-13

Abstract Dihydroorotate dehydrogenase (DHODH) is an enzyme involved in the biosynthesis of pyrimidine nucleotides. In most eukaryotes, this bound to inner mitochondrial membrane, where it couples synthesis orotate with reduction ubiquinone. As ubiquinone must be regenerated by respiratory complex III, and cellular respiration are tightly coupled. Consequently, inhibition leads cessation DNA impairs cell proliferation. We show that expression Saccharomyces cerevisiae URA1 gene ( ScURA )...

10.1101/2024.08.09.607333 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-08-09

Respiratory complex I plays a crucial role in the mitochondrial electron transport chain and shows promise as therapeutic target for various human diseases. While most studies focus on inhibiting at Q-site, little is known about inhibitors targeting other sites within complex. In this study, we demonstrate that diphenyleneiodonium (DPI), N-site inhibitor, uniquely affects stability of by reacting with its flavin cofactor FMN. Treatment DPI blocks final stage assembly, leading to complete...

10.1016/j.redox.2023.103001 article EN cc-by-nc-nd Redox Biology 2023-12-20

TET-family members play an essential role in cell fate commitment and their dysfunctions result arrested differentiation. TET3 is ubiquitously expressed differentiated cells postnatal development due to yet unknown reasons. To define function differentiation, we profiled the intestinal epithelium at single-cell level from wild-type Tet3 knockout mice. Here show that, absence of TET3, enterocytes exhibit aberrant differentiation trajectory do not acquire a physiological identity impairment...

10.1101/2024.01.23.576868 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-01-24

TET-family members play a critical role in cell fate commitment. Indeed, TET3 is essential to postnatal development due yet unknown reasons. To define function differentiation, we have profiled the intestinal epithelium at single-cell level from wild-type and Tet3 knockout mice. We found that mostly expressed differentiated enterocytes. In absence of TET3, enterocytes exhibit an aberrant differentiation trajectory do not acquire physiological identity impairment oxidative phosphorylation,...

10.1038/s41467-024-54044-0 article EN cc-by-nc-nd Nature Communications 2024-11-18
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