ReviewAnnals of intensive care2024
Impaired angiotensin II signaling in septic shock.
Review in Annals of intensive care, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Early multimodal vasopressor strategy in septic shock: results of the TRICYCLE randomized controlled trial.Critical care (London, England) · 2026Trial
- Clinical trials testing early multimodal vasopressor therapy require a dose ceiling, not a dose floor.Critical care (London, England) · 2026Article
- Beyond the Pump: Unravelling Immunometabolic Crosstalk and Organelle Dynamics in Sepsis-Induced Cardiomyopathy.Journal of cardiovascular translational research · 2026Article
- Current and future strategies aiming at reducing catecholamine exposure in septic shock.Critical care (London, England) · 2026Review
- The balance between classical and alternative renin-angiotensin system in ARDS: a narrative review.Journal of intensive care · 2026Review
- Toward endotype-guided renin-angiotensin-aldosterone system modulation in septic shock.Critical care (London, England) · 2026Article
- Prognosis of critically ill patients with severe acute kidney injury and high circulating dipeptidyl peptidase 3: a post hoc analysis of the AKIKI 2 trial.Critical care (London, England) · 2026Article
- Novel aspects of the renin-angiotensin-aldosterone system in septic shock.Current opinion in physiology · 2026Article
- Targeting the renin-angiotensin system in sepsis-associated AKI: from pathophysiology to precision medicine.Frontiers in immunology · 2026Review
- Targeting high circulating dipeptidyl peptidase 3 in circulatory failure.Critical care (London, England) · 2025Review
- Alterations in the renin-angiotensin system during septic shock.Annals of intensive care · 2025Article
- Higher circulating ACE2 and DPP3 but reduced ACE and angiotensinogen in hyperreninemic sepsis patients.Clinical science (London, England : 1979) · 2025Article
- Early multimodal vasopressor strategy in septic shock (TRICYCLE)-Study protocol for a randomized controlled clinical trial.PloS one · 2025Article
- Alterations in the Renin-Angiotensin System in Experimental Septic Shock.Critical care explorations · 2024Article
- Clinical Outcomes of Angiotensin II Therapy in Vasoplegic Shock: A Systematic Review and Meta-Analysis.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent years have seen a resurgence of interest for the renin-angiotensin-aldosterone system in critically ill patients. Emerging data suggest that this vital homeostatic system, which plays a crucial role in maintaining systemic and renal hemodynamics during stressful conditions, is altered in septic shock, ultimately leading to impaired angiotensin II-angiotensin II type 1 receptor signaling. Indeed, available evidence from both experimental models and human studies indicates that alterations in the renin-angiotensin-aldosterone system during septic shock can occur at three distinct levels: 1. Impaired generation of angiotensin II, possibly attributable to defects in angiotensin-converting enzyme activity; 2. Enhanced degradation of angiotensin II by peptidases; and/or 3. Unavailability of angiotensin II type 1 receptor due to internalization or reduced synthesis. These alterations can occur either independently or in combination, ultimately leading to an uncoupling between the renin-angiotensin-aldosterone system input and downstream angiotensin II type 1 receptor signaling. It remains unclear whether exogenous angiotensin II infusion can adequately address all these mechanisms, and additional interventions may be required. These observations open a new avenue of research and offer the potential for novel therapeutic strategies to improve patient prognosis. In the near future, a deeper understanding of renin-angiotensin-aldosterone system alterations in septic shock should help to decipher patients' phenotypes and to implement targeted interventions.
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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.