Biocommunication in Cardiometabolic Medicine

Publication 2026

Published on in News

Mimouni et al. Journal of Translational Medicine 2026

Leroy et al. Antioxidants 2026

Revel et al. *Emerging Microbes & Infections*, 2026

At the start of 2026, the BC2M team published three scientific articles in leading international journals, demonstrating the dynamism and excellence of its research activities.

Mimouni M, Darlet S, Jover B, Gayrard N, Jeanson L, Blanchard MP, Lajoix AD, Desmetz C. Involvement of Fibulin-5 in the endothelial-to-mesenchymal transition leading to cardiac fibrosis during metabolic syndrome. J Transl Med. July 7, 2026. doi: 10.1186/s12967-026-08589-x. Published online ahead of print. PMID: 42415085.

"Cardiac fibrosis is a hallmark of metabolic syndrome, a condition linked to Western lifestyles and high cardiovascular risk. We previously demonstrated that dietary sodium restriction prevents cardiac fibrosis and remodeling in a rat model of metabolic syndrome by reducing macrophage infiltration. Here, we investigate genes involved in endothelial-to-mesenchymal transition (EndoMT), a key process in cardiac fibrosis."

Leroy J, Mezghenna K, Tousch D, Canovas J, Laune D, Pugnière M, Azay-Milhau J, Lajoix AD. PIN (Protein Inhibitor of Neuronal Nitric Oxide Synthase) Modulates Glucose Uptake Through NO-Dependent and Independent Mechanisms in Rat Muscle Cells. Antioxidants (Basel). March 31, 2026;15(4):436. doi: 10.3390/antiox15040436. PMID: 42072078; PMCID: PMC13114162.

"Protein inhibitor of neuronal NO synthase (PIN), also known as dynein light chain 8 (LC8), is a highly conserved protein that interacts with multiple partners, such as neuronal NO synthase (nNOS) and myosin Va, to modulate a variety of cellular functions. Since PIN is expressed in skeletal muscle, our goal was to investigate a possible role of PIN in glucose uptake in L6 and primary muscle cells. Overexpression of PIN resulted in decreased glucose uptake, accompanied by reduced GLUT4 expression and translocation to the plasma membrane—similar to the effects of pharmacological blockade of nNOS with L-NAME. The effect of PIN is mediated by a reduction in nNOS protein levels and a direct interaction with nNOS, leading to reduced NO production in L6 myocytes. Surprisingly, siRNA targeting PIN decreased glucose uptake and GLUT4 translocation, suggesting the involvement of nNOS-independent effects. We therefore focused on myosin Va, which interacts with PIN in L6 myocytes. Silencing myosin Va caused a decrease in glucose uptake. Since PIN siRNA also reduced myosin Va expression, this confirms the essential role of myosin Va in the observed effects of PIN silencing on glucose uptake. We conclude that PIN modulates glucose uptake and GLUT4 translocation in rat muscle cells through both NO-dependent and NO-independent mechanisms.”

Revel J, Leroy J, Delbecq S, Constant O, Henry Marty F, Naili C, Barthès A, Nagy A, Schmidt-Chanasit J, Cadar D, Abd Rahaman NY, Lajoix AD, Desmetz C, Simonin Y. Differential properties of NS1 glycoproteins in West Nile and Usutu viruses. Emerg Microbes Infect. Dec 2026;15(1):2667565. doi: 10.1080/22221751.2026.2667565. Epub May 29, 2026. PMID: 42054312; PMCID: PMC13224725.

“West Nile virus (WNV) and Usutu virus (USUV) are neurotropic orthoflaviviruses of the Flaviviridae family, transmitted primarily by Culex mosquitoes and maintained in enzootic cycles involving birds. While WNV is a well-established human pathogen causing hundreds of neuroinvasive cases annually in Europe, USUV has emerged more recently, with fewer documented human infections but increasing evidence of neurovirulence. The viral nonstructural protein 1 (NS1) plays a central role in orthoflavivirus pathogenesis by modulating host immune responses, disrupting endothelial barrier integrity, and facilitating viral dissemination. However, the functional and biochemical properties of NS1 from WNV and USUV remain poorly characterized. We combined in vitro, in vivo, and clinical approaches to compare NS1 secretion, stability, and its impact on the blood-brain barrier. Our results show that WNV NS1 is secreted at significantly higher levels, exhibits greater thermal stability, and disrupts the integrity of the brain endothelial barrier in vitro. In contrast, USUV NS1 is secreted less efficiently, is slightly less stable, and does not compromise the integrity of the blood-brain barrier, despite inducing distinct transcriptional responses in brain endothelial cells. In mice, WNV infection led to higher serum NS1 levels and stronger systemic inflammation than USUV. Clinically, WNV NS1 was detected mainly in patients with neurological symptoms, whereas USUV NS1 remained undetectable in all cases. Taken together, these findings reveal differences in NS1 properties between these closely related viruses, with key implications for orthoflavivirus diagnosis and neurovirulence mechanisms.”