Evidence map›Paper›PMID 40558557›Full record

ReviewCells2025

Inflammasomes and Signaling Pathways: Key Mechanisms in the Pathophysiology of Sepsis.

Jhan S Saavedra-Torres, María Virginia Pinzón-Fernández, Martin Ocampo-Posada, H A Nati-Castillo, Laura Alejandra Jiménez Hincapie, Eder J Cadrazo-Gil, Marlon Arias-Intriago, Marlon Rojas-Cadena, Andrea Tello-De-la-Torre, Walter Osejos and 1 more

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

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  13. From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Jhan S Saavedra-TorresGrupo de Investigación en Salud (GIS), Universidad del Cauca, Popayan 190002, Colombia.ORCID 0009-0002-3643-1737
María Virginia Pinzón-FernándezGrupo de Investigación en Salud (GIS), Universidad del Cauca, Popayan 190002, Colombia.
Martin Ocampo-PosadaGrupo de Investigación en Ciencias Básicas y Clínicas de la Salud, Universidad Javeriana, Cali 760031, Colombia.ORCID 0000-0001-7154-3692
H A Nati-CastilloInterinstitutional Group of Internal Medicine (GIMI I), Universidad Libre, Cali 760031, Colombia.ORCID 0000-0003-1890-4983
Laura Alejandra Jiménez HincapieFacultad de Medicina, Fundación Universitaria Autónoma de las Américas, Pereira 660003, Colombia.ORCID 0009-0002-7448-4063
Eder J Cadrazo-GilFacultad de Medicina, Universidad del Norte, Barranquilla 081007, Colombia.
Marlon Arias-IntriagoOne Health Research Group, Universidad de las Américas, Quito 170124, Ecuador.ORCID 0009-0002-3717-383X
Marlon Rojas-CadenaOne Health Research Group, Universidad de las Américas, Quito 170124, Ecuador.ORCID 0000-0002-8445-7256
Andrea Tello-De-la-TorreOne Health Research Group, Universidad de las Américas, Quito 170124, Ecuador.ORCID 0000-0002-5927-8600
Walter OsejosDepartamento de Medicina Interna, Clínica Guayaquil, Guayaquil 090313, Ecuador.ORCID 0000-0002-7834-1863
Juan S Izquierdo-CondoyOne Health Research Group, Universidad de las Américas, Quito 170124, Ecuador.ORCID 0000-0002-1178-0546

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a life-threatening syndrome characterized by a dysregulated immune response to infection, frequently leading to multiorgan failure and high mortality. Inflammasomes-cytosolic multiprotein complexes of the innate immune system-serve 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-1β and IL-18 maturation, and gasdermin D-mediated 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.

Indexed as

InflammasomesSepsisSignal TransductionAnimalsHumansPyroptosisInflammasomescoagulationcytokinesimmunomodulationinflammasomepyroptosissepsis

Identifiers

PMID40558557
PMCPMC12191029

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.