What is the clinical evidence from this study?

Population: Diabetes. Intervention: Pin1 up-regulation vs. Healthy controls / Pin1(-/-) mice. Primary outcome: Mitochondrial oxidative stress, endothelial dysfunction, and vascular inflammation.

What question did this study set out to answer?

To determine the role of the prolyl-isomerase Pin1 in driving diabetes-induced vascular dysfunction and inflammation.

April 28, 2026European Heart JournalOpen Access

Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes

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Key result

Pin1 inhibition prevents diabetic vascular dysfunction by reducing mitochondrial oxidative stress and inflammation.

Why the study?

Diabetes is a major driver of cardiovascular disease, but the underlying mechanisms involving prolyl-isomerase Pin1 remain elusive.

Does targeting prolyl-isomerase Pin1 prevent mitochondrial oxidative stress and vascular dysfunction in diabetes models?

Population

Human aortic endothelial cells, diabetic Pin1(-/-) mice, and peripheral blood monocytes from diabetic patients and healthy controls

Comparison

Pin1 gene silencing or knockout vs control conditions or wild-type

Design

Preclinical experimental study

Authors

FPFrancesco PaneniPreventive Cardiology SCSarah CostantinoHeart Failure & Transplant LCLorenzo CastelloUniversity of Milano-Bicocca

Discussion

Member takes

Implication

Targeting Pin1 may prevent diabetic vascular disease by reducing mitochondrial oxidative stress and endothelial dysfunction.

Key Points

To determine the role of the prolyl-isomerase Pin1 in driving diabetes-induced vascular dysfunction and inflammation.
Treated human aortic endothelial cells (HAECs) with high glucose, analyzing the effects of Pin1 silencing on p66(Shc) translocation, eNOS activity, and NF-κB signaling.
Evaluated vascular inflammation, mitochondrial oxidative stress, and endothelial dysfunction in diabetic Pin1-knockout mice compared to wild-type controls.
Isolated peripheral blood monocytes from diabetic patients and healthy controls to quantify Pin1 expression, plasma adhesion molecules, urinary 8-iso-prostaglandin F2α, and flow-mediated dilation.
High glucose in HAECs increased Pin1 expression, which promoted mitochondrial p66(Shc) translocation, impaired eNOS function, and induced NF-κB nuclear translocation; Pin1 silencing completely reversed these defects.
Diabetic Pin1-knockout mice were protected against mitochondrial oxidative stress, vascular inflammation, and endothelial dysfunction.
Patients with diabetes displayed elevated monocyte Pin1 expression and activity, which correlated with impaired flow-mediated dilation, elevated urinary 8-iso-prostaglandin F2α, and increased plasma adhesion molecules.

Structured PICO

Does targeting prolyl-isomerase Pin1 prevent mitochondrial oxidative stress and vascular dysfunction in diabetes models?

Population

Human aortic endothelial cells (HAECs), diabetic Pin1(-/-) mice, and peripheral blood monocytes from diabetic patients and age-matched healthy controls

Exposure

Pin1 gene silencing (in vitro) and Pin1 knockout (in vivo)

Comparator

Control conditions (high glucose without silencing, wild-type diabetic mice, healthy human controls)

Outcome

Mitochondrial oxidative stress, endothelial dysfunction, and vascular inflammationsurrogate

Targeting Pin1 may prevent diabetic vascular disease by reducing mitochondrial oxidative stress and endothelial dysfunction.

Cite This Study

Paneni et al. (2014) studied Diabetes. Pin1 up-regulation vs. Healthy controls / Pin1(-/-) mice was evaluated on Mitochondrial oxidative stress, endothelial dysfunction, and vascular inflammation. Pin1 up-regulation in diabetes drives vascular disease by causing mitochondrial oxidative stress, eNOS dysregulation, and NF-kB-induced inflammation.

synapsesocial.com/papers/69f0cfedb606b7e8fdeb2f4a https://doi.org/10.1093/eurheartj/ehu179

View Full Paper

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Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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