The Role of Altreded Gut Mierobiota in Cardiovascular Diasese
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Date
2020
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Rīgas Stradiņa universitāte
Rīga Stradiņš University
Rīga Stradiņš University
Abstract
Sirds un asinsvadu slimības (SAS) ir vadošās neinfekcijas slimības visā pasaulē, jau ilgi tiek meklēti veidi, kā efektīvi identificēt un novērst jaunus mainīgus SAS riska faktorus. Zarnu mikrobiota ir viena no kuņģa-zarnu trakta veselīgajām sastāvdaļām, tai ir ne tikai fizioloģiska loma, bet arī būtiska loma aterosklerozes un SAS patoģenēze.
Lai pētītu zarnu mikrobiotas lomu SAS, šajā pētījumā tiks analizēta literatūra un klīniskie pētījumi. Zarnu mikrobiotas komponentus raksturo metagenomika, taču zarnu disbiozes jēdzienam ir mazinājusies nozīme, jo zarnu mikrobiotas metabolīt izraisa saslimšanu.
Zarnu mikrobiotas metabolīta Trimetilamīna N-oksīds (“TMAO”) kā anterogēnas vielas un SAS veicināšanas atklāšana var tikt uzskatīta kā liels panākums pētījums par zarnu mikrobiotas lomu SAS. Īsās ķēdes taukskābes (“SCFAs”), fenilacetilglutamīns (“PAG”) un sekundārās žultsskābes, kas darbojas uz konkrētiem receptoriem, un citi no zarnu mikrobiotas iegūti metabolīti ir saistīti ar SAS.
Zarnu noplūde un lipopolisaharīda (“LPS”) klātbūtne sistemātiski var veicināt endotēlija ievainojumus un iekaisums, un šie faktori kopā ar patogēniem zarnu mikrobiotas metabolītiem veicina aterosklerozi, izraisot koronāro artēriju slimību, insultu, miokarda infarktu, perifēro artēriju slimību, sirds mazspēju un pat 2. tipa cukura diabētu.
Visbeidzot, ir vairāki iejaukšanās veidi, kuri ir būtiski, modificē zarnu mikrobiotu un tās metabolītus, tādējādi samazinot SAS risku kā - prebiotikas, probiotikas, enzīmu inhibitori, fekāliju mikrobu transplantācijas un izmaiņas uzturā. Tomēr, lai varētu veikt lielus panākumus zarnu mikrobiotas un tās metabolītu mērķtiecīgai noteikšanai, lai novērstu SAS, ir jāveic vairāk pētījumu.
Cardiovascular diseases (CVDs) are the leading non-communicable diseases worldwide and there has been a long search to find and target new modifiable risk factors of CVD. Gut microbiota (GM) are normal components of our gastrointestinal tract and are increasingly found to have not only physiologic roles, as they also are found to have substantial roles in the development of atherosclerosis and CVD. To address the role of GM in CVD, this review formulated a search strategy to find relevant publications of GM-mediated pathogenesis in CVD. Normal GM components have been better characterized by metagenomics, however the concept of gut dysbiosis seems to be of decreased importance, as it is rather the GM metabolites that mediate disease and not the diversity of the GM itself. The discovery of the GM metabolite Trimethylamine N-oxide (TMAO) as an atherogenic substance and promotor of CVD can be thought of as an evolution in the study of the role of GM in disease. Short-chain fatty acids (SCFA), phenylacetylglutamine, and secondary bile acids which work act specific receptors, and other GM-derived metabolites all have been associated with CVD. Gut leakiness and the presence of lipopolysaccharide (LPS) systemically can cause further enhance injury to the endothelium, and together with pathogenic GM metabolites these factors all contribute to atherosclerosis, causing coronary artery disease (CAD), stroke, myocardial infarction (MI), peripheral artery disease (PAD), heart failure, and even type 2 diabetes mellitus (T2DM). Finally, there are several forms of interventions which have been of proposed value in altering the GM and their metabolites to convey a decreased risk of CVD, including prebiotics, probiotics, bacterial enzyme inhibitors, faecal microbial transplants (FMT), and changes in diet. However, more investigation is needed before large steps can be made in targeting GM and its metabolites to prevent CVD.
Cardiovascular diseases (CVDs) are the leading non-communicable diseases worldwide and there has been a long search to find and target new modifiable risk factors of CVD. Gut microbiota (GM) are normal components of our gastrointestinal tract and are increasingly found to have not only physiologic roles, as they also are found to have substantial roles in the development of atherosclerosis and CVD. To address the role of GM in CVD, this review formulated a search strategy to find relevant publications of GM-mediated pathogenesis in CVD. Normal GM components have been better characterized by metagenomics, however the concept of gut dysbiosis seems to be of decreased importance, as it is rather the GM metabolites that mediate disease and not the diversity of the GM itself. The discovery of the GM metabolite Trimethylamine N-oxide (TMAO) as an atherogenic substance and promotor of CVD can be thought of as an evolution in the study of the role of GM in disease. Short-chain fatty acids (SCFA), phenylacetylglutamine, and secondary bile acids which work act specific receptors, and other GM-derived metabolites all have been associated with CVD. Gut leakiness and the presence of lipopolysaccharide (LPS) systemically can cause further enhance injury to the endothelium, and together with pathogenic GM metabolites these factors all contribute to atherosclerosis, causing coronary artery disease (CAD), stroke, myocardial infarction (MI), peripheral artery disease (PAD), heart failure, and even type 2 diabetes mellitus (T2DM). Finally, there are several forms of interventions which have been of proposed value in altering the GM and their metabolites to convey a decreased risk of CVD, including prebiotics, probiotics, bacterial enzyme inhibitors, faecal microbial transplants (FMT), and changes in diet. However, more investigation is needed before large steps can be made in targeting GM and its metabolites to prevent CVD.
Description
Medicīna
Medicine
Veselības aprūpe
Health Care
Medicine
Veselības aprūpe
Health Care
Keywords
Sirds un asinsvadu slimības, mainīgus SAS riska faktorus, Zarnu mikrobiota, aterosklerozes, SAS patoģenēze, koronāro artēriju, LPS, zarnu disbiozes, prebiotikas, Zarnu mikrobiotas metabolīta, fekāliju mikrobu transplan, Trimetilamīna N-oksīds, TMAO, Īsās ķēdes taukskābes, SCFA, fenilacetilglutamīns, Cardiovascular disease, modifiable risk factors, gut microbiota, atherosclerosis, cardiovascular disease pathogenesis, coronary artery disease, LPS, gut dysbiosis, prebiotics, faecal microbial transplants (FMT), TMAO, Short-chain fatty acids (SCFA), phenylacetylglutamine, secondary bile acids, MI.