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Related Experiment Video

Updated: May 15, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Telmisartan modulates mitochondrial function in vascular smooth muscle cells.

Kiyo Takeuchi¹, Koichi Yamamoto, Mitsuru Ohishi

¹Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Hypertension Research : Official Journal of the Japanese Society of Hypertension

|December 21, 2012

Summary

Telmisartan improves mitochondrial function in vascular smooth muscle cells (VSMCs) by enhancing adenosine triphosphate (ATP) production and reducing apoptosis. These effects on mitochondria are key to understanding cardiovascular disease pathogenesis.

Related Experiment Videos

Last Updated: May 15, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Area of Science:

Cardiovascular Biology
Mitochondrial Medicine
Pharmacology

Background:

Atherosclerosis involves mitochondrial dysfunction in vascular smooth muscle cells (VSMCs), leading to impaired ATP production, increased superoxide generation, and apoptosis.
Peroxisome proliferator-activated receptor gamma (PPARγ) plays a role in regulating mitochondrial metabolism.

Purpose of the Study:

To investigate the effects of telmisartan, a partial PPARγ agonist and angiotensin receptor blocker, on mitochondria-related cellular responses in VSMCs.
To determine if telmisartan's effects on mitochondrial function are mediated by PPARγ activation.

Main Methods:

Human VSMCs were treated with telmisartan or eprosartan.
Mitochondrial function markers, including ATP levels, mitochondrial complex II activity, and hydrogen peroxide (H2O2) release, were assessed.
Apoptosis was measured by caspase 3/7 activity.
Experiments were conducted in both normal and PPARγ-deficient VSMCs.

Main Results:

Telmisartan increased ATP levels and mitochondrial complex II activation in VSMCs.
Telmisartan reduced H2O2 release and attenuated H2O2-induced apoptosis.
Eprosartan, lacking PPARγ activation, had no significant effects.
Telmisartan's effects on mitochondrial function were largely independent of PPARγ, though PPARγ modulated H2O2 levels.

Conclusions:

Telmisartan significantly impacts mitochondrial metabolism in VSMCs, independent of solely acting through angiotensin receptor blockade or PPARγ activation.
These findings suggest telmisartan's potential relevance in cardiovascular disease pathogenesis due to its beneficial effects on mitochondrial function.