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A study has identified a new molecular mechanismbased on the interaction between a microRNA and a regulatory proteinthat controls inflammation of the arteries in diabetes and that could become a future therapeutic target in front of the atherosclerosis.
The researchers consider that this finding is keysince the atherosclerosis acts as a progressive hardening of the arteries due to the accumulation of fatty plaques. In people with diabetesthese injuries tend to be more inflammatory and unstablewhich increases the risk of cardiovascular events such as heart attack or stroke.
The work, published in the magazine Cardiovascular Diabetologyis led by Carmen Gomez-Guerrero and counts as first signatories with Mary Kavanagh and Isabel Herreroresearchers in the area of CIBER Diabetes and Associated Metabolic Diseases (CIBERDEM) in it Jiménez Díaz Foundation Health Research Institute (IIS-FJD) and the Autonomous University of Madrid.
The study reveals, according to Europa Press, that during the progression of atherosclerosis there is a inverse relationship between these two molecules. “We have observed that, as the vascular injury progresses, the levels of microRNA miR-155-5p increase, while the expression of the Socs1 protein —a powerful natural inflammation brake— decreases,” explained Gómez-Guerrero.
According to the specialist, this balance disturbance is especially relevant in the diabetes. The increase of miR-155-5p favors the inflammatory activation of macrophages and vascular smooth muscle cells and, at the same time, reduces the ability to remove dead cells on the plate, a process called efferocytosis. As a consequence, the lesion may grow and become more unstableincreasing the risk of rupture.
To analyze the role of this molecular axisthe team performed experiments in diabetic mice with a predisposition to develop atherosclerosis. In these models they applied two strategies: block the action of the microRNA miR-155-5p either increase Socs1 levels through gene transfer.
Both approaches had similar effects. The treated animals presented smaller atherosclerotic lesions and with characteristics of greater stabilityas lower lipid content and greater presence of collagen.
The work also reveals that this mechanism affects the efferocytosisthe process by which macrophages remove dead cells inside the atherosclerotic plaque. When this system fails, the cellular debris accumulates and favor the formation of a necrotic corewhich increases fragility of the injury.
The research staff verified that miR-155-5p interferes with MerTK receptor functiona key molecule for this cell cleaning is carried out correctly. To the inhibit microRNAthe efferocytosis improves and it reduces the expansion of the necrotic core.
Possible therapeutic implications
The results identify the miR-155-5p/Socs1 shaft like a relevant regulator of vascular inflammation associated with diabetes and suggest that their modulation could have therapeutic interest. “These findings indicate that acting on this molecular axis could not only reduce vascular inflammationbut also enhance natural repair mechanisms of the arteries,” he points out. Carmen Gomez-Guerrerostudy coordinator.
Although it is a preclinical studythe research team highlights that the results reinforce the potential of therapies targeting microRNAs as complementary strategy to the current treatments for prevent cardiovascular disease in people with diabetes.
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