Jankauskas, Stanislovas S, Urna Kansakar, Fahimeh Varzideh, and Gaetano Santulli. “IL-33 Drives Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension.”. Hypertension (Dallas, Tex. : 1979) 83, no. 2 (2026): e26356. https://doi.org/10.1161/HYPERTENSIONAHA.125.26356.
Publications by Year: 2026
2026
Sommella, Eduardo Maria, Concetta Iside, Paola Di Pietro, Fabrizio Merciai, Emanuela Salviati, Marina Sala, Angela Carmelita Abate, et al. “Lysolecithin Reprogramming via LPCAT1 Modulation Restores Endothelial Function and Prevents Diabetes-Associated Dysmetabolism.”. Cardiovascular Diabetology, 2026. https://doi.org/10.1186/s12933-025-03053-4.
BACKGROUND: Dysregulation of lysophosphatidylcholines (LPCs) and phosphatidylcholines (PCs) is linked to endothelial dysfunction and impaired tissue repair. Nevertheless, the organ-specific modulation of lysolecithin remodeling in T2DM remains unexplored. Here, we investigate the LPC/PC remodeling dynamics in a T2DM model and propose a novel therapeutic approach using an orally bioavailable peptide (SP6) derived from Spirulina platensis.
METHODS: LPC/PC levels were analyzed by UHPLC-HRMS. Membrane fluidity, VEGF/API5, LPCAT1, VE-cadherin, and GLUT1 were evaluated by merocyanine assay, qPCR, immunoblotting, and immunofluorescence. In vivo, T2DM was induced by a high-fat diet and streptozotocin, and SP6 was orally administered. Tissue lipidomics, GLUTs expression, and insulin secretion were assessed, with the latter also spatially characterized in pancreatic tissue by MALDI-MS imaging.
RESULTS: High glucose induced LPC/PC imbalance, enhanced membrane fluidity, impaired VEGF/API5 expression, and hindered wound healing and VE-cadherin localization via LPCAT1 downregulation and subsequent impact on GLUT1 translocation. In vivo analysis of diabetic mice revealed a multi-organ influence of SP6 preserving LPCAT1 mRNA levels in pancreas, liver, skeletal muscle, and adipose tissue and a specific pattern of lysolecithin remodeling, with selective modulation of LPC 16:0, 18:0, and 20:4 in plasma. Finally, its effects in T2DM are mediated by preserving insulin secretion and glycemic control through increased ATP production.
CONCLUSION: These findings reveal tissue-specific lysolecithin reprogramming in T2DM development and identify LPCAT1-mediated lysolecithin remodeling as a mechanism involved in T2DM-related endothelial and metabolic dysfunction. SP6 modulates lipid metabolism, vascular integrity, and glucose regulation at the transcript level, suggesting its potential as a new preventive treatment for T2DM and its complications.
Varzideh, Fahimeh, Pasquale Mone, and Gaetano Santulli. “A New Proteomic Clock Links Accelerated Ageing to Ischaemic Stroke: No Country for Old Vessels.”. European Journal of Preventive Cardiology, 2026. https://doi.org/10.1093/eurjpc/zwag023.
Jankauskas, Stanislovas S, Urna Kansakar, Pasquale Mone, Fahimeh Varzideh, and Gaetano Santulli. “Like a Rolling Tone: Ablating LRRC8A Eases Inflammation and Keeps Vessels Moving.”. Hypertension (Dallas, Tex. : 1979) 83, no. 1 (2026): 54-56. https://doi.org/10.1161/HYPERTENSIONAHA.125.26261.