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Translational evidence of prothrombotic and inflammatory endothelial damage in Cushing syndrome after remission
Gloria Aranda1,2, Rebeca Fernandez-Ruiz3, Marta Palomo4,5
1Group of Endocrine Disorders, IDIBAPS, Barcelona, Spain.
Insights
Even after Cushing syndrome (CS) remission, persistent cardiovascular risk factors are present. Sera from women with remitted CS show pro-inflammatory and prothrombotic effects on endothelium, increasing cardiovascular risk.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Translational Research
Background:
- Observational studies suggest a persistent cardiovascular risk phenotype after Cushing syndrome (CS) remission.
- Understanding the underlying mechanisms is crucial for managing long-term health outcomes in these patients.
Purpose of the Study:
- To evaluate the subclinical cardiometabolic burden in active CS and CS in remission (RCS).
- To explore the direct pro-inflammatory and prothrombotic potential of sera from CS patients on endothelial cells in vitro.
Main Methods:
- A cross-sectional study involving three groups: RCS (n=9), active CS (ACS, n=9), and controls (CTR, n=9).
- In vivo assessments included cardiometabolic profile, endothelial markers, endothelial dysfunction (FMD), intima-media thickness, and body composition (DEXA).
- In vitro experiments exposed endothelial cells (EC) to patient sera to assess inflammatory response (tisVCAM-1) and thrombogenicity (VWF, platelet reactivity).
Main Results:
- Active CS patients exhibited typical metabolic features.
- RCS patients showed statistically significant increases in Hs-CRP compared to controls.
- In vitro, sera from both ACS and RCS groups induced increased inflammatory markers (tisVCAM-1), VWF, and platelet adhesion on extracellular matrix compared to controls.
Conclusions:
- Sera from premenopausal women with remitted CS contain circulatory factors that exert direct pro-inflammatory and prothrombotic effects on the endothelium.
- These endothelial effects may contribute to the increased cardiovascular risk observed in patients after CS remission.
Objective:
Sustained evidence from observational studies indicates that after remission of Cushing syndrome (CS) a cardiovascular risk phenotype persists. Here, we performed a translational study in active CS and CS in remission (RCS) to evaluate the subclinical cardiometabolic burden and to explore the direct pro-inflammatory and prothrombotic potential of their sera on the endothelium in an in vitro translational atherothrombotic cell model.
Patients:
Cross sectional study. The groups were (n = 9/group): I. RCS; II. Active CS (ACS) and III. Controls (CTR), all matched for age, body mass index, sex, without other hormonal deficits.
Design:
We evaluated in vivo: cardiometabolic profile; endothelial markers (sVCAM-1, NO); endothelial dysfunction (FMD); intima-media thickness and body composition (DEXA). In vitro endothelial cells (EC) were exposed to sera taken from the different subjects to evaluate inflammatory EC response (tisVCAM) and thrombogenicity of the generated extracellular matrix (ECM): von Willebrand factor (VWF) and platelet reactivity.
Results:
Three of the 9 RCS subjects were on glucocorticoid replacement therapy (GC-RT). Patients on GC-RT had a shorter period of time in stable remission. In vivo analysis ACS showed typically metabolic features, while cardiometabolic markers reached statistical significance for RCS only for Hs-CRP (P < .01). In vitro:EC exposed to ACS and RCS sera displayed increased tisVCAM-1 (P < .01 for ACS and P < .05 for RCS vs CTR), VWF (P < .01 for ACS and P < .05 for RCS vs CTR) and platelet adhesion on ECM (P < .01 for ACC and P < .05 for RCS vs CTR). No statistically significant differences were observed between GC-RT RSC and RCS without GC-RT.
Conclusions:
The sera of premenopausal women with CS in remission, without atherothrombotic disease, contain circulatory endothelial deleterious factors with a direct thrombogenic and pro-inflammatory endothelial effect that could increase cardiovascular risk.
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