Heart fail­ure study shows pro­tein block­age could im­prove car­diac func­tion

Tehran Times - - SCI / MED -

An ex­per­i­ment con­ducted in mice showed that car­dio­vas­cu­lar func­tion can be im­proved just by block­ing a par­tic­u­lar pro­tein in the heart. The ther­apy proved suc­cess­ful in mouse models, al­though fur­ther re­search is war­ranted in hu­man heart cells.

An ex­per­i­men­tal study done in mice shows a po­ten­tial for pre­vent­ing heart fail­ure and im­prov­ing car­diac func­tion by block­ing a pro­tein type.

Re­searchers at the Cincin­nati Chil­dren’s Heart In­sti­tute ex­per­i­mented on a tar­geted molec­u­lar ther­apy that blocks fi­bronectin pro­tein, which over­re­acts at the time of a heart at­tack.

Fi­bronectin func­tions as a cell ad­he­sive that binds to­gether col­la­gen and other proteins es­sen­tial for the mi­gra­tion, growth, and dif­fer­en­ti­a­tion of heart cells.

Cell ad­he­sion comes in the form of ma­tri­ces that con­nect tis­sues, es­pe­cially af­ter an in­jury. Un­for­tu­nately, af­ter a car­diac ar­rest, the fi­bronectin over­re­acts and over­pro­duces con­nec­tive ma­tri­ces. It also causes clog­ging that even­tu­ally dam­age the heart.

De­ceased pa­tients

Us­ing a do­nated heart by de­ceased pa­tients, the re­searchers man­u­fac­tured a pep­tide called pUR4 to in­hibit fi­bronectin from over­pro­duc­ing con­nec­tive tis­sues.

“Our data are a strong proof of prin­ci­ple and the first to show that in­hibit­ing fi­bronectin poly­mer­iza­tion pre­serves heart func­tion, re­duces left ven­tri­cle re­mod­el­ing, and lim­its the for­ma­tion of fi­brotic con­nec­tive tis­sue,” said lead au­thor Dr. Burns Blax­all, di­rec­tor of trans­la­tional re­search at the Heart In­sti­tute and the Cen­ter for Trans­la­tional Fi­bro­sis Re­search.

The re­searchers re­ported that in­hibit­ing fi­bronectin from over­pro­duc­ing ma­trix tis­sues can pre­vent heart fail­ure and even im­prove car­diac func­tions.

Few ef­fec­tive op­tions are avail­able to treat heart dis­eases, es­pe­cially for peo­ple who had pre­vi­ous at­tacks or have con­gen­i­tal con­di­tions. In­di­vid­u­als who were born with con­gen­i­tal heart dis­eases re­quire spe­cial­ized care even when they reach adult­hood.

Blax­all’s team has opened the study to fu­ture in­ves­ti­ga­tions on the ap­pli­ca­tion of pUR4 in hu­man heart cells. The study, which was pub­lished in the jour­nal Cir­cu­la­tion, used mouse models in a sim­u­lated heart at­tack. The an­i­mals then de­vel­oped fi­bro­sis and even­tu­ally had heart fail­ure.

Is­chemic heart dis­ease

About 54 per­cent of mor­tal­ity rate or 15 mil­lion deaths in 2015 are at­trib­uted to is­chemic heart dis­ease and stroke, ac­cord­ing to World Health Or­ga­ni­za­tion.

Clin­i­cians rec­om­mend life­style mod­i­fi­ca­tion as one of the strong­est forms of in­ter­ven­tion in re­duc­ing risks of heart dis­ease. Seden­tary life­style, smok­ing, obe­sity, and other causative events are iden­ti­fied as ad­verse fac­tors.

In a mul­ti­cen­ter, ran­dom­ized trial funded by the Na­tional Heart, Lung, and Blood In­sti­tute, 810 adults with Level 1 hy­per­ten­sion were ad­mit­ted to a non-phar­ma­co­logic pro­gram.

Par­tic­i­pants were in­volved in DASH diet and an es­tab­lished in­ter­ven­tion group. The EST group gave in­di­vid­ual ad­vice on phys­i­cal ac­tiv­i­ties, weight loss, in­clud­ing caloric, al­co­hol, and sodium in­take for a pe­riod of six months.

As a re­sult, the DASH and EST in­ter­ven­tions have low­ered the prob­a­bil­ity of a

10-year risk for coro­nary heart dis­ease by

12 to 14 per­cent.

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