Loading
Life sciences · Journal article
Biomolecules · August 8, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review article synthesizing current knowledge of enolase-1 as a multifunctional protein implicated in inflammatory pathways across multiple diseases including sepsis, ARDS, and rheumatoid arthritis. The source proposes compartment-specific roles of ENO-1 and identifies it as a therapeutic target, but does not present new empirical data or clinical trial results.
Journal article. Patients and biological systems with inflammatory diseases including sepsis, acute respiratory distress syndrome, acute organ injury, hemorrhagic shock, rheumatoid arthritis, and cancer.
ENO-1 regulates macrophage inflammation during sepsis via cytosolic function ENO-1 functions as a plasminogen receptor on the cell surface and participates in innate immune signaling extracellularly ENO-1 has been implicated in sepsis, acute respiratory distress syndrome, acute organ injury, hemorrhagic shock, rheumatoid arthritis, and cancer-associated inflammation
No quantitative effect sizes, clinical trial outcomes, or safety data are reported Therapeutic targeting approaches are mentioned but no efficacy or safety results are provided
The review suggests ENO-1 is a significant therapeutic target in inflammatory disease, but does not provide evidence that targeting ENO-1 changes clinical outcomes. Clinicians should regard this as a framework for understanding potential mechanisms rather than actionable clinical guidance.
This is a narrative review synthesizing mechanistic evidence and existing literature on ENO-1's role in inflammation, raising questions about compartment-specific therapeutic targeting rather than reporting new empirical evidence.
The review suggests ENO-1 is a significant therapeutic target in inflammatory disease, but does not provide evidence that targeting ENO-1 changes clinical outcomes. Clinicians should regard this as a framework for understanding potential mechanisms rather than actionable clinical guidance.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Enolase-1 (ENO-1) is classically known as a highly conserved glycolytic enzyme that catalyzes the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the final steps of glycolysis. This enzyme, however, is being increasingly implicated as a multifunctional moonlighting protein with compartment-specific roles in inflammation. Within the cytosol, ENO-1 regulates macrophage inflammation during sepsis; on the cell surface, it functions as a plasminogen receptor, and extracellularly, it can participate in innate immune signaling. Across innate and adaptive immunity, ENO-1 has been implicated in macrophage activation, neutrophil recruitment, endothelial cell dysfunction, fibroblast remodeling, and autoantigenicity. These functions have been linked to sepsis, acute respiratory distress syndrome, acute organ injury, hemorrhagic shock, rheumatoid arthritis, and cancer-associated inflammation in the tumor microenvironment. Therapeutic targeting of ENO-1 includes small-molecule inhibitors and monoclonal antibodies. ENO-1, with its compartment-specific functions in disease pathogenesis, serves as a significant therapeutic target for inflammatory diseases. In this review, we discuss the novel compartment-specific roles of ENO-1 in inflammatory diseases, defining its functions beyond its role in glycolysis. We conclude that both the metabolic and moonlighting functions of ENO-1 contribute to inflammation, and future studies should delineate its compartment-specific roles in inflammatory pathophysiology, as compartment-specific targeting may represent the future of ENO-1-directed therapy.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.