ArticleFrontiers in immunology2018
Deterioration of Organ Function As a Hallmark in Sepsis: The Cellular Perspective.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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.
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Who cites it
27 citing papers in PubMed, 32 citations in OpenAlex.
- Novel Adipokines in Critical Illness and Sepsis: Chemerin, Vaspin, and Omentin-1: A Comprehensive Evidence-Based Review.Biomedicines · 2026Review
- Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps contribute significantly to vascular dysfunction in sepsis.Frontiers in pharmacology · 2026Review
- Subphenotyping sepsis based on organ interaction trajectory using a deep temporal graph clustering model: a retrospective cohort study.EClinicalMedicine · 2025Article
- Sepsis toxicity network reconstruction-Dynamic signaling and multi-organ injury: A review.Biomolecules & biomedicine · 2025Review
- The progress of organ protection mechanisms in sepsis.Frontiers in immunology · 2025Review
- Compartmentalization of the inflammatory response during bacterial sepsis and severe COVID-19.Journal of intensive medicine · 2024Review
- Article
- Review
- Exploiting the Zebrafish Model for Sepsis Research: Insights into Pathophysiology and Therapeutic Potentials.Drug design, development and therapy · 2024Review
- Controversies Surrounding Albumin Use in Sepsis: Lessons from Cirrhosis.International journal of molecular sciences · 2023Review
- Roquin-1 resolves sepsis-associated acute liver injury by regulating inflammatory profiles via miRNA cargo in extracellular vesicles.iScience · 2023Article
- A pharmacoproteomic landscape of organotypic intervention responses in Gram-negative sepsis.Nature communications · 2023Article
- Altered EEG, disrupted hippocampal long-term potentiation and neurobehavioral deficits implicate a delirium-like state in a mouse model of sepsis.Brain, behavior, and immunity · 2023Article
- Mesenchymal stem cell-derived exosome alleviates sepsis- associated acute liver injury by suppressing MALAT1 through microRNA-26a-5p: an innovative immunopharmacological intervention and therapeutic approach for sepsis.Frontiers in immunology · 2023Article
- The liver in sepsis: molecular mechanism of liver failure and their potential for clinical translation.Molecular medicine (Cambridge, Mass.) · 2022Review
- Tidy up - The unfolded protein response in sepsis.Frontiers in immunology · 2022Review
- Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations.International journal of molecular sciences · 2021Review
- Circular RNA circFADS2 is overexpressed in sepsis and suppresses LPS-induced lung cell apoptosis by inhibiting the maturation of miR-15a-5p.BMC immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of organ dysfunction discriminates sepsis from uncomplicated infection. The paradigm shift implicated by the new sepsis-3 definition holds that initial impairment of any organ can pave the way for multiple organ dysfunction and death. Moreover, the role of the systemic inflammatory response, central element in previous sepsis definitions, has been questioned. Most strikingly, a so far largely underestimated defense mechanism of the host, i.e., "disease tolerance," which aims at maintaining host vitality without reducing pathogen load, has gained increasing attention. Here, we summarize evidence that a dysregulation of critical cellular signaling events, also in non-immune cells, might provide a conceptual framework for sepsis-induced dysfunction of parenchymal organs in the absence of significant cell death. We suggest that key signaling mediators, such as phosphoinositide 3-kinase, mechanistic target of rapamycin, and AMP-activated protein kinase, control the balance of damage and repair processes and thus determine the fate of affected organs and ultimately the host. Therapeutic targeting of these multifunctional signaling mediators requires cell-, tissue-, or organ-specific approaches. These novel strategies might allow stopping the domino-like damage to further organ systems and offer alternatives beyond the currently available strictly supportive therapeutic options.
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Registered trials
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 OpenQuestion graph.