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In the heart, an inhibited protein cures heart failure

2022-09-22T15:15:03.338Z


The SGLT2 protein is present in heart cells and increases in diabetic patients. Responsible for the heart's energy inefficiency, this protein facilitates the development of heart failure. (HANDLE)


The SGLT2 protein is present in heart cells and increases in diabetic patients.

Responsible for the heart's energy inefficiency, this protein facilitates the development of heart failure.

It is the result of a joint research conducted by Raffaele Marfella of the Vanvitelli University and by Ciro Maiello of the Monaldi Hospital, published in the scientific journal Pharmacological Research.



 The research carried out both on cardiac biopsies of 67 heart transplant patients, and in cell cultures of humanized cardiomyocytes, has shown the presence of SGLT2 thus opening new scenarios for the efficacy of therapies.

"Recently - explains Raffaele Marfella professor at the Vanvitelli University - numerous pharmacological trials had shown that inhibitors of this protein (glyphozine), in addition to improving metabolic compensation in diabetics, were able to improve cardiac performance by reducing the risk of heart failure. in patients with and without diabetes, but it was not clear how these drugs act in the heart. Today, however, we have a clearer picture ".

    The study demonstrates not only the presence of the SGLT2 protein in heart cells, whose concentration is accentuated by hyperglycemia, but also that the ability to increase the use of glucose but not that of lipids in cardiac cells is to be considered a mechanism which reduces the energy efficiency and therefore the contraction capacity of these cells.

    "The importance of this research - concludes Giuseppe Paolisso, professor at Vanvitelli and coordinator of the study - allows us to understand how glyphzines are effective in the therapy of heart failure in non-diabetic and diabetic patients, but above all to identify for the first time in man a specific cardiac pharmacological mechanism in addition to the extra-cardiac ones known up to now ".

(HANDLE).


Source: ansa

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