STIM1-dependent treg dysfunction promotes cardiometabolic heart failure with preserved ejection fraction (HFpEF): insights from patients and animal studies
Authors' conclusion
STIM1-dependent stress signaling drives maladaptive Treg instability that amplifies cardiovascular inflammation and HFpEF progression.
Study context
- Population
- Patients with and without HFpEF (circulating Tregs); mice on high-fat diet plus nitric oxide synthase inhibition (L-NAME) as a cardiometabolic HFpEF model
- Comparison
- Patients with vs without HFpEF; TregStim1-/- mice vs littermate controls
- Outcome
- Tregs in HFpEF and effect of Treg STIM1 deletion
Methodological detailshuman and animal studies, Treg-specific STIM1 deletion, littermate controls, high-fat diet plus L-NAME HFpEF model
- Human and animal studies
- Treg-specific STIM1 deletion
- Littermate controls
- High-fat diet plus L-NAME HFpEF model
Main finding
As reported in the abstract
- Patients with HFpEF: reduced circulating Treg numbers, increased STIM1 expression and activation of apoptotic, inflammatory and ER stress pathways
- Control mice developed HFpEF features: diastolic dysfunction with preserved ejection fraction, hypertension, metabolic dysregulation, endothelial dysfunction, cardiac fibrosis, impaired exercise tolerance
- TregStim1-/- mice were protected from these abnormalities
- STIM1 signaling promoted loss of Treg suppressive stability and effector-like inflammatory signaling, incl. IL-17- and IFN-γ-dependent cardiomyocyte activation; STIM1-deficient Tregs kept a non-pathogenic phenotype
Original publication
STIM1-dependent treg dysfunction promotes cardiometabolic HFpEF: insights from patients and animal studies. Cardiovasc Diabetol. Published 8 July 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →