Publications by authors named "S Garbay"
Article Synopsis
- * The study reveals that HNF1β remains attached to chromatin during both interphase and mitosis in a specific manner, aided by a protein called BTBD2 that activates Topoisomerase 1 (TOP1) during mitosis.
- * A mutation associated with "maturity onset diabetes of the young" can disrupt the interaction between HNF1β and TOP1, highlighting HNF1β's key role in chromatin remodeling and gene reactivation, which is essential for maintaining cellular identity after cell division.
Acute kidney injury is one of the most important complications in patients with COVID-19 and is considered a negative prognostic factor with respect to patient survival. The occurrence of direct infection of the kidney by SARS-CoV-2, and its contribution to the renal deterioration process, remain controversial issues. By studying 32 renal biopsies from patients with COVID-19, we verified that the major pathological feature of COVID-19 is acute tubular injury (ATI).
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- The shape of nephrons, which are tiny units in the kidneys, is really important for how well the kidneys work.
- Scientists used a special method that combines different techniques to better see and understand these nephrons in 3D.
- They found that in a kidney disease model, cysts formed in specific areas of the nephrons, and their shapes varied depending on where they were located.
The architecture of renal glomeruli is acquired through intricate and still poorly understood developmental steps. In our study we identify a crucial glomerular morphogenetic event in nephrogenesis that drives the remodeling/separation of the prospective vascular pole (the future entrance of the glomerular arterioles) and the urinary pole (the tubular outflow). We demonstrate that this remodeling is genetically programmed.
View Article and Find Full Text PDFThe loss of functional nephrons after kidney injury triggers the compensatory growth of the remaining ones to allow functional adaptation. However, in some cases, these compensatory events activate signaling pathways that lead to pathological alterations and chronic kidney disease. Little is known about the identity of these pathways and how they lead to the development of renal lesions.
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