eprintid: 17835 rev_number: 6 eprint_status: archive userid: 2 dir: disk0/00/01/78/35 datestamp: 2025-09-05 23:30:15 lastmod: 2025-09-05 23:30:15 status_changed: 2025-09-05 23:30:15 type: article metadata_visibility: show creators_name: Rezabakhsh, Aysa creators_name: Safaei, Nasser creators_name: Nabavi, Seyed Mohammad creators_name: Roosta, Yousef creators_name: Giampieri, Francesca creators_name: Battino, Maurizio creators_id: creators_id: creators_id: creators_id: creators_id: francesca.giampieri@uneatlantico.es creators_id: maurizio.battino@uneatlantico.es title: Anti-atherogenic immune checkpoint TIM-3 as a promising pharmacologic target toward ischemic heart diseases: a prospective review ispublished: pub subjects: uneat_bm divisions: uneatlantico_produccion_cientifica full_text_status: none keywords: Immune checkpoint inhibitors; Ischemic heart diseases Inflammatory heart disease; Systemic inflammatory reaction syndrome (SIRS); T-cell immunoglobulin and mucin domain 3 abstract: Recently, immunogene therapy has been of great interest in cardiovascular diseases. In this regard, various immune checkpoint inhibitors (ICIs) are identified to have a crucial role in regulating inflammatory responses. The T-cell immunoglobulin and mucin-domain containing molecule-3 (TIM-3, CD366), a relatively newly discovered group of molecules with a conserved structure, has emerged as a critical immune checkpoint with significant regulatory roles in cardiovascular inflammation and atherosclerosis. This prospective review explores the importance of TIM-3 in modulating immune responses relevant to ischemic heart diseases (IHD), highlighting its interactions with inflammatory pathways such as Toll-like receptor-4 (TLR-4). TIM-3, predominantly expressed on T cells, dendritic cells, and monocytes, acts as an inhibitory receptor that quenches pro-inflammatory signaling, particularly upon binding to ligands like galectin-9. Noteworthy, recent evidence suggests that TIM-3 deficiency or dysregulation can exacerbate inflammatory cascades, contributing to the progression of IHD and related complications. Here, the therapeutic potential of targeting TIM-3 for the management of IHD, especially in the settings of systemic inflammation and post-operative complications, has been discussed. By elucidating the molecular mechanisms and translational prospects of TIM-3 modulation, this work proposes new avenues for immunotherapeutic intervention in cardiovascular disease and post-operative SIRS, warranting further research in clinical trials. date: 2025-06 publication: Molecular Biology Reports volume: 52 number: 1 id_number: doi:10.1007/s11033-025-10729-3 refereed: TRUE issn: 0301-4851 official_url: http://doi.org/10.1007/s11033-025-10729-3 access: close language: en citation: Artículo Materias > Biomedicina Universidad Europea del Atlántico > Investigación > Artículos y libros Cerrado Inglés Recently, immunogene therapy has been of great interest in cardiovascular diseases. In this regard, various immune checkpoint inhibitors (ICIs) are identified to have a crucial role in regulating inflammatory responses. The T-cell immunoglobulin and mucin-domain containing molecule-3 (TIM-3, CD366), a relatively newly discovered group of molecules with a conserved structure, has emerged as a critical immune checkpoint with significant regulatory roles in cardiovascular inflammation and atherosclerosis. This prospective review explores the importance of TIM-3 in modulating immune responses relevant to ischemic heart diseases (IHD), highlighting its interactions with inflammatory pathways such as Toll-like receptor-4 (TLR-4). TIM-3, predominantly expressed on T cells, dendritic cells, and monocytes, acts as an inhibitory receptor that quenches pro-inflammatory signaling, particularly upon binding to ligands like galectin-9. Noteworthy, recent evidence suggests that TIM-3 deficiency or dysregulation can exacerbate inflammatory cascades, contributing to the progression of IHD and related complications. Here, the therapeutic potential of targeting TIM-3 for the management of IHD, especially in the settings of systemic inflammation and post-operative complications, has been discussed. By elucidating the molecular mechanisms and translational prospects of TIM-3 modulation, this work proposes new avenues for immunotherapeutic intervention in cardiovascular disease and post-operative SIRS, warranting further research in clinical trials. metadata Rezabakhsh, Aysa; Safaei, Nasser; Nabavi, Seyed Mohammad; Roosta, Yousef; Giampieri, Francesca y Battino, Maurizio mail SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, francesca.giampieri@uneatlantico.es, maurizio.battino@uneatlantico.es (2025) Anti-atherogenic immune checkpoint TIM-3 as a promising pharmacologic target toward ischemic heart diseases: a prospective review. Molecular Biology Reports, 52 (1). ISSN 0301-4851