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Sökning: WFRF:(Chakaroun Rima 1983) > The potential of ta...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004340naa a2200445 4500
001oai:gup.ub.gu.se/320692
003SwePub
008240528s2023 | |||||||||||000 ||eng|
024a https://gup.ub.gu.se/publication/3206922 URI
024a https://doi.org/10.1038/s41569-022-00771-02 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Chakaroun, Rima,d 1983u Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberg Laboratory,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xchrim
2451 0a The potential of tailoring the gut microbiome to prevent and treat cardiometabolic disease
264 c 2022-10-14
264 1b Springer Science and Business Media LLC,c 2023
520 a In this Review, Backhed and colleagues summarize the evidence for gut microbiome alterations in cardiometabolic and cardiovascular diseases and the rationale and potential benefit motivating translational approaches to target the gut microbiota and its metabolites for prevention and treatment. Despite milestones in preventive measures and treatment, cardiovascular disease (CVD) remains associated with a high burden of morbidity and mortality. The protracted nature of the development and progression of CVD motivates the identification of early and complementary targets that might explain and alleviate any residual risk in treated patients. The gut microbiota has emerged as a sentinel between our inner milieu and outer environment and relays a modified risk associated with these factors to the host. Accordingly, numerous mechanistic studies in animal models support a causal role of the gut microbiome in CVD via specific microbial or shared microbiota-host metabolites and have identified converging mammalian targets for these signals. Similarly, large-scale cohort studies have repeatedly reported perturbations of the gut microbial community in CVD, supporting the translational potential of targeting this ecological niche, but the move from bench to bedside has not been smooth. In this Review, we provide an overview of the current evidence on the interconnectedness of the gut microbiome and CVD against the noisy backdrop of highly prevalent confounders in advanced CVD, such as increased metabolic burden and polypharmacy. We further aim to conceptualize the molecular mechanisms at the centre of these associations and identify actionable gut microbiome-based targets, while contextualizing the current knowledge within the clinical scenario and emphasizing the limitations of the field that need to be overcome.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
653 a chain fatty-acids
653 a trimethylamine-n-oxide
653 a incident cardiovascular
653 a events
653 a protein-coupled receptor
653 a randomized double-blind
653 a coronary-heart-disease
653 a metabolic syndrome
653 a intestinal microbiota
653 a dietary fiber
653 a all-cause
653 a Cardiovascular System & Cardiology
700a Olsson, Lisa M.,d 1984u Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberg Laboratory,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xollit
700a Bäckhed, Fredrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory4 aut0 (Swepub:gu)xbafre
710a Göteborgs universitetb Wallenberglaboratoriet4 org
773t Nature Reviews Cardiologyd : Springer Science and Business Media LLCg 20:4, s. 217-235q 20:4<217-235x 1759-5002x 1759-5010
8564 8u https://gup.ub.gu.se/publication/320692
8564 8u https://doi.org/10.1038/s41569-022-00771-0

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