New potential pathway to treat cocaine’s cardiovascular harm

New York, Feb 27 (IANS) Scientists have found a potential new pathway that can help treat the harmful effects of cocaine on the cardiovascular system.

Cocaine abuse can increase blood pressure, cause aortic stiffening -- a hardening of arteries -- as well as raise the risk of cardiovascular mortality and morbidity.

The study found that cocaine introduction increased the levels of reactive oxygen species (ROS), molecules known to be found in the aortas of hypertensive animals and humans.

A build-up of ROS species in cells may contribute to illness, ageing and, damage to the body's heart and blood vessel system.

"The discovery of this novel cocaine pathway provides a potential new therapeutic avenue for treatment of cocaine abuse-related (cardiovascular) disease," said scientists including Chunming Dong, Professor at the University of Miami, in the US.

For the study, published in the journal Hypertension, the team used a mouse model for cocaine abuse/use.

They found that repeated cocaine injection led to increased blood pressure and aortic stiffness in mice associated with elevated levels of ROS in the aortas -- a phenomenon similar to that observed in hypertensive humans.

They found that cocaine activates the molecule microRNA (miR)-30c-5p, increasing the levels of ROS in the cardiovascular system.

But, blocking activation of miR-30c-5p dramatically reduced cocaine-induced cardiovascular impacts, the researchers noted.

"The biggest surprise to us was that the modulation of a single miRNA-mRNA pathway could have such a profound effect on cardiovascular function," Dong explained.

"This also suggests that targeting this one pathway may have significant therapeutic benefit, which is an exciting possibility," Dong added.

The team plans to test the findings to see if they are observed in human patients to determine the viability of this targeted pathway.

(This story has not been edited by Social News XYZ staff and is auto-generated from a syndicated feed.)

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