{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T22:41:02Z","timestamp":1792190462874,"version":"4.4.0"},"reference-count":161,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T00:00:00Z","timestamp":1750291200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Sepsis is a life-threatening syndrome characterized by a dysregulated immune response to infection, frequently leading to multiorgan failure and high mortality. Inflammasomes\u2014cytosolic multiprotein complexes of the innate immune system\u2014serve as critical platforms for sensing pathogen- and damage-associated molecular patterns (PAMPs and DAMPs). Key sensors such as NLRP3, AIM2, and IFI16 initiate caspase-1 activation, IL-1\u03b2 and IL-18 maturation, and gasdermin D\u2013mediated pyroptosis. In sepsis, excessive inflammasome activation drives oxidative stress, endothelial dysfunction, immunothrombosis, and immune exhaustion. This maladaptive cascade is further aggravated by the release of DAMPs and procoagulant factors, compromising vascular integrity and immune homeostasis. Prolonged activation contributes to immunoparalysis, lymphopenia, and increased susceptibility to secondary infections. Inflammasome signaling also intersects with necroptosis and ferroptosis, amplifying systemic inflammation and tissue injury. Additionally, various pathogens exploit immune evasion strategies to modulate inflammasome responses and enhance virulence. Therapeutic interventions under investigation include selective NLRP3 inhibitors, IL-1 blockers, gasdermin D antagonists, and extracorporeal cytokine hemoadsorption. Emerging approaches emphasize biomarker-guided immunomodulation to achieve personalized therapy. While preclinical studies have shown promising results, clinical translation remains limited. Targeting inflammasomes may offer a path toward precision immunotherapy in sepsis, with potential to reduce organ dysfunction and improve survival.<\/jats:p>","DOI":"10.3390\/cells14120930","type":"journal-article","created":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T09:57:48Z","timestamp":1750327068000},"page":"930","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Inflammasomes and Signaling Pathways: Key Mechanisms in the Pathophysiology of Sepsis"],"prefix":"10.3390","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-3643-1737","authenticated-orcid":false,"given":"Jhan S.","family":"Saavedra-Torres","sequence":"first","affiliation":[{"name":"Grupo de Investigaci\u00f3n en Salud (GIS), Universidad del Cauca, Popayan 190002, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda Virginia","family":"Pinz\u00f3n-Fern\u00e1ndez","sequence":"additional","affiliation":[{"name":"Grupo de Investigaci\u00f3n en Salud (GIS), Universidad del Cauca, Popayan 190002, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7154-3692","authenticated-orcid":false,"given":"Martin","family":"Ocampo-Posada","sequence":"additional","affiliation":[{"name":"Grupo de Investigaci\u00f3n en Ciencias B\u00e1sicas y Cl\u00ednicas de la Salud, Universidad Javeriana, Cali 760031, Colombia"},{"name":"Interinstitutional Group of Internal Medicine (GIMI I), Universidad Libre, Cali 760031, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1890-4983","authenticated-orcid":false,"given":"H. A.","family":"Nati-Castillo","sequence":"additional","affiliation":[{"name":"Interinstitutional Group of Internal Medicine (GIMI I), Universidad Libre, Cali 760031, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-7448-4063","authenticated-orcid":false,"given":"Laura Alejandra","family":"Jim\u00e9nez Hincapie","sequence":"additional","affiliation":[{"name":"Facultad de Medicina, Fundaci\u00f3n Universitaria Aut\u00f3noma de las Am\u00e9ricas, Pereira 660003, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eder J.","family":"Cadrazo-Gil","sequence":"additional","affiliation":[{"name":"Facultad de Medicina, Universidad del Norte, Barranquilla 081007, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-3717-383X","authenticated-orcid":false,"given":"Marlon","family":"Arias-Intriago","sequence":"additional","affiliation":[{"name":"One Health Research Group, Universidad de las Am\u00e9ricas, Quito 170124, Ecuador"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8445-7256","authenticated-orcid":false,"given":"Marlon","family":"Rojas-Cadena","sequence":"additional","affiliation":[{"name":"One Health Research Group, Universidad de las Am\u00e9ricas, Quito 170124, Ecuador"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5927-8600","authenticated-orcid":false,"given":"Andrea","family":"Tello-De-la-Torre","sequence":"additional","affiliation":[{"name":"One Health Research Group, Universidad de las Am\u00e9ricas, Quito 170124, Ecuador"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7834-1863","authenticated-orcid":false,"given":"Walter","family":"Osejos","sequence":"additional","affiliation":[{"name":"Departamento de Medicina Interna, Cl\u00ednica Guayaquil, Guayaquil 090313, Ecuador"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1178-0546","authenticated-orcid":false,"given":"Juan S.","family":"Izquierdo-Condoy","sequence":"additional","affiliation":[{"name":"One Health Research Group, Universidad de las Am\u00e9ricas, Quito 170124, Ecuador"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,6,19]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"417","DOI":"10.1016\/S1097-2765(02)00599-3","article-title":"The Inflammasome: A Molecular Platform Triggering Activation of Inflammatory Caspases and Processing of proIL-\u03b2","volume":"10","author":"Martinon","year":"2002","journal-title":"Mol. 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