A monoterpene widely found in several essential oils called 1,8-cineole or eucalyptol decreased right ventricular hypertrophy and fibrosis and improved heart function in a mouse model with pulmonary arterial hypertension (PAH), according to a new study published in Pharmacological Research.

“Overall, our results point out a promising therapeutic compound that can be easily applied topically, thus paving the way for the development of effective cardiac-specific therapies to greatly improve PAH outcomes,” first author Jorge M. Alves-Silva and the coauthors of the study wrote.

The mortality rate of patients with PAH is still very high and is mainly associated with right ventricular dysfunction. This is a study that describes a therapeutic approach for PAH that is specific to the heart.

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The team of researchers led by HenriqueGirão, PhD, from the Coimbra Institute for Clinical and Biomedical Research in Portugal, first developed a new in vitro model of hypertrophy induced by high pressure, which is similar to heart defects seen in the PAH model. They also used a mouse model of PAH induced by monocrotaline to validate the findings they obtained using the in vitro model.

They saw that 1,8-cineole had an antihypertrophic effect in vitro. It also accumulated in the heart of diseased mice where it led to a decrease in right ventricular hypertrophy and improved heart function.

The researchers also found that 1,8-cineole restored the distribution of the gap junction protein connexin 43 at the intercalated discs and improved the functionality of the mitochondria. This suggests that 1,8-cineole may function by preserving cell-cell communication and bioenergetics in the heart, the researchers said.

1,8-cineole is mainly found in Eucalyptus globulus. It has previously been shown to have hypotensive and vasodilator properties.


Alves-Silva JM, Zuzarte M, Marques C, et al. 1,8-cineole ameliorates right ventricle dysfunction associated with pulmonary arterial hypertension by restoring connexin 43 and mitochondrial homeostasis. Pharmacol Res. 2022;2:106151. doi:10.1016/j.phrs.2022.106151