Inflammasomes and Signaling Pathways: Key Mechanisms in the Pathophysiology of Sepsis Article Swipe
Jhan Sebastián Saavedra-Torres
,
María Virginia Pinzón Fernández
,
Martín Ocampo-Posada
,
Humberto Alejandro Nati-Castillo
,
Laura Alejandra Jiménez Hincapie
,
Eder J. Cadrazo-Gil
,
Marlon Arias-Intriago
,
Marlon Rojas-Cadena
,
Andrea Tello-De-la-Torre
,
Walter Osejos
,
Juan S. Izquierdo‐Condoy
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.3390/cells14120930
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.3390/cells14120930
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.
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Metadata
- Type
- review
- Language
- en
- Landing Page
- https://doi.org/10.3390/cells14120930
- https://www.mdpi.com/2073-4409/14/12/930/pdf?version=1750327360
- OA Status
- gold
- Cited By
- 5
- References
- 162
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4411451760
All OpenAlex metadata
Raw OpenAlex JSON
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https://openalex.org/W4411451760Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.3390/cells14120930Digital Object Identifier
- Title
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Inflammasomes and Signaling Pathways: Key Mechanisms in the Pathophysiology of SepsisWork title
- Type
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reviewOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-06-19Full publication date if available
- Authors
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Jhan Sebastián Saavedra-Torres, María Virginia Pinzón Fernández, Martín Ocampo-Posada, Humberto Alejandro Nati-Castillo, Laura Alejandra Jiménez Hincapie, Eder J. Cadrazo-Gil, Marlon Arias-Intriago, Marlon Rojas-Cadena, Andrea Tello-De-la-Torre, Walter Osejos, Juan S. Izquierdo‐CondoyList of authors in order
- Landing page
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https://doi.org/10.3390/cells14120930Publisher landing page
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https://www.mdpi.com/2073-4409/14/12/930/pdf?version=1750327360Direct link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://www.mdpi.com/2073-4409/14/12/930/pdf?version=1750327360Direct OA link when available
- Concepts
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Pathophysiology, Signal transduction, Sepsis, Neuroscience, Medicine, Biology, Cell biology, Immunology, PathologyTop concepts (fields/topics) attached by OpenAlex
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5Total citation count in OpenAlex
- Citations by year (recent)
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2025: 5Per-year citation counts (last 5 years)
- References (count)
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162Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.infection, | 12 |
| abstract_inverted_index.intersects | 110 |
| abstract_inverted_index.mortality. | 20 |
| abstract_inverted_index.multiorgan | 16 |
| abstract_inverted_index.strategies | 127 |
| abstract_inverted_index.virulence. | 134 |
| abstract_inverted_index.Therapeutic | 135 |
| abstract_inverted_index.activation, | 52 |
| abstract_inverted_index.contributes | 97 |
| abstract_inverted_index.dysfunction | 188 |
| abstract_inverted_index.endothelial | 69 |
| abstract_inverted_index.exhaustion. | 74 |
| abstract_inverted_index.infections. | 106 |
| abstract_inverted_index.inhibitors, | 142 |
| abstract_inverted_index.maladaptive | 76 |
| abstract_inverted_index.maturation, | 56 |
| abstract_inverted_index.necroptosis | 112 |
| abstract_inverted_index.preclinical | 162 |
| abstract_inverted_index.pyroptosis. | 60 |
| abstract_inverted_index.translation | 169 |
| abstract_inverted_index.D–mediated | 59 |
| abstract_inverted_index.Inflammasome | 107 |
| abstract_inverted_index.antagonists, | 147 |
| abstract_inverted_index.compromising | 89 |
| abstract_inverted_index.dysfunction, | 70 |
| abstract_inverted_index.dysregulated | 8 |
| abstract_inverted_index.ferroptosis, | 114 |
| abstract_inverted_index.homeostasis. | 94 |
| abstract_inverted_index.inflammasome | 64, 130 |
| abstract_inverted_index.inflammation | 117 |
| abstract_inverted_index.lymphopenia, | 100 |
| abstract_inverted_index.multiprotein | 22 |
| abstract_inverted_index.personalized | 159 |
| abstract_inverted_index.procoagulant | 87 |
| abstract_inverted_index.Additionally, | 121 |
| abstract_inverted_index.characterized | 5 |
| abstract_inverted_index.immunotherapy | 180 |
| abstract_inverted_index.inflammasomes | 173 |
| abstract_inverted_index.interventions | 136 |
| abstract_inverted_index.investigation | 138 |
| abstract_inverted_index.extracorporeal | 149 |
| abstract_inverted_index.susceptibility | 103 |
| abstract_inverted_index.system—serve | 28 |
| abstract_inverted_index.hemoadsorption. | 151 |
| abstract_inverted_index.biomarker-guided | 155 |
| abstract_inverted_index.immunomodulation | 156 |
| abstract_inverted_index.immunoparalysis, | 99 |
| abstract_inverted_index.life-threatening | 3 |
| abstract_inverted_index.damage-associated | 36 |
| abstract_inverted_index.immunothrombosis, | 71 |
| abstract_inverted_index.Inflammasomes—cytosolic | 21 |
| cited_by_percentile_year.max | 98 |
| cited_by_percentile_year.min | 97 |
| corresponding_author_ids | https://openalex.org/A5021976866 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 11 |
| corresponding_institution_ids | https://openalex.org/I4210102282 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.8500000238418579 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.97148593 |
| citation_normalized_percentile.is_in_top_1_percent | True |
| citation_normalized_percentile.is_in_top_10_percent | True |