Job offer

Organisation/Company INSERM Nice Research Field Biological sciences » Biology Biological sciences » Biology Researcher Profile Recognised Researcher (R2) Leading Researcher (R4) First Stage Researcher (R1) Established Researcher (R3) Application Deadline 22 Mar 2026 - 22:00 (UTC) Type of Contract Temporary Job Status Full-time Offer Starting Date 27 Sep 2026 Is the job funded through the EU Research Framework Programme? Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No

Offer Description

Metabolic dysfunction–associated steatohepatitis is a leading cause of liver fibrosis, cirrhosis, and hepatocellular carcinoma. Hepatocyte injury initiates fibrogenesis, yet how stressed hepatocytes transmit pathogenic signals to neighboring cells remains poorly understood.

Work from Dr Bailly-Maitre’s team shows that hepatocyte-specific inhibition of IRE1αRNase activity protects against liver fibrosis (Hazari et al, Hepatology 2026). In parallel, our data indicate that ER-stress components are released in the hepatocyte secretome and transferred to hepatocytes and hepatic stellate cells, promoting disease progression. Emerging evidence from Dr Chami’s laboratory gain expertise in extracellular vesicles (EVs) studies in Alzheimer’s disease (Lauritzen et al., J Extracellular Vesicles 2025; Eysert et al., DOI: ). Theydemonstrate that stressed cells export dysfunctional mitochondria through large EVs containing mitochondria, propagating metabolic stress between cells. They develop reliable protocols for small and large EVs isolation from tissuesin vivo.

This PhD project will test whether hepatocyte-derived EVs act as vectors of ER-stress signals and mitochondrial dysfunction, thereby amplifying fibrogenesis. Using genetically engineered mouse models targeting hepatocyte IRE1αRNase activity, combined with EVs isolation and proteomic characterization, mitochondrial transfer assays, and metabolic profiling, we will define how EVs cargo reprograms recipient hepatocytes and HSCs.

The project relies on a complementary collaboration between a team specialized in liver biology, ER stress and fibrosis and a team expert in EVs and mitochondrial biology. Beyond liver pathology, we will explore whether chronic hepatocyte stress and EV-mediated mitochondrial dissemination contribute to cognitive alterations, building on Dr Chami’s expertise in neurodegenerative diseases and data linking hepatocyte RNase activity to systemic inflammation.

Candidate Profile

• current Master’s student (M2 – class of 2026)
• Master’s graduate from the class of 2025, ideally with distinction.

National and international applications are welcome.

Our laboratory has a strong international outlook, and the PhD project may include a research stay of approximately one month in a leading partner laboratory related to the project — for example in Chile — through an international scientific exchange program.