Genetic Programming of Hypertension

Ahn, Sun Young; Gupta, Charu

doi:10.3389/fped.2017.00285

Cited by 31 publications

(24 citation statements)

References 103 publications

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“…Dysregulation of multiple contributing factors has been demonstrated in hypertension 80 , including the reninangiotensin system 81,82 , the ANS 82,83 and the immune system 84 . Environmental factors in association with epi-genetic 85 and genetic 86 components have critical roles in the initiation, maintenance and progression of hyper-tension. In addition, emerging evidence indicates that the gut microbiota has an essential role in hypertension development.…”

Section: The Gut Microbiota In Hypertensionmentioning

confidence: 99%

The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease

et al. 2018

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Crosstalk between the gut microbiota and the host has attracted considerable attention owing to its involvement in diverse diseases. Chronic kidney disease (CKD) is commonly associated with hypertension and is characterized by immune dysregulation, metabolic disorder and sympathetic activation, which are all linked to gut dysbiosis and altered host-microbiota crosstalk. In this Review, we discuss the complex interplay between the brain, the gut, the microbiota and the kidney in CKD and hypertension and explain our brain-gut-kidney axis hypothesis for the pathogenesis of these diseases. Consideration of the role of the brain-gut-kidney axis in the maintenance of normal homeostasis and of dysregulation of this axis in CKD and hypertension could lead to the identification of novel therapeutic targets. In addition, the discovery of unique microbial communities and their associated metabolites and the elucidation of brain-gut-kidney signalling are likely to fill fundamental knowledge gaps leading to innovative research, clinical trials and treatments for CKD and hypertension.

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Section: The Gut Microbiota In Hypertensionmentioning

confidence: 99%

The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease

et al. 2018

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“…Different genes have been involved in the development of AH, including CACANA1H, IPO7, PMS1, SLC24A4, YWHAZ, GPR98, ARRDC3, C21orf, SLC25A42, genes HLA-B, inter alia. Among those involved with T2DM the following have been identified: SLC44A3, F3, RBM43, RND3, GALNTL4, CPA6, LOC729013, and 7-like 2 transcription factor (TCF7L2), with is strongly associated with the development of T2DM in several ethnic groups [ 32 , 33 , 34 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Control of blood pressure and cardiovascular outcomes in type 2 diabetes

Vargas‐Uricoechea

Cáceres-Acosta

2018

Open Medicine

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AbstractHigh blood pressure in patients with diabetes mellitus results in a significant increase in the risk of cardiovascular events and mortality. The current evidence regarding the impact of intervention on blood pressure levels (in accordance with a specific threshold) is not particularly robust. Blood pressure control is more difficult to achieve in patients with diabetes than in non-diabetic patients, and requires using combination therapy in most patients. Different management guidelines recommend initiating pharmacological therapy with values >140/90 mm/Hg; however, an optimal cut point for this population has not been established. Based on the available evidence, it appears that blood pressure targets will probably have to be lower than <140/90mmHg, and that values approaching 130/80mmHg should be recommended. Initial treatment of hypertension in diabetes should include drug classes demonstrated to reduce cardiovascular events; i.e., angiotensin converting-enzyme inhibitors, angiotensin receptor blockers, diuretics, or dihydropyridine calcium channel blockers. The start of therapy must be individualized in accordance with the patient's baseline characteristics, and factors such as associated comorbidities, race, and age, inter alia.

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“…Over the last decade, diagnosis of LS has dramatically improved as a direct result of an increase in our knowledge of the genetic mutations underlying sporadic and familial forms of the disease [31]. LS diagnosis is based on clinical characteristics and genetic evidence.…”

Section: Discussionmentioning

confidence: 99%

Premature Stroke Secondary to Severe Hypertension Results from Liddle Syndrome Caused by a Novel SCNN1B Mutation

Fan

Zhang

Pan

et al. 2020

Kidney Blood Press Res

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Introduction: Liddle syndrome (LS), an autosomal dominant and inherited monogenic hypertension syndrome caused by pathogenic mutations in the epithelial sodium channel (ENaC) genes SCNN1A, SCNN1B, and SCNN1G. Objective: This study was designed to identify a novel SCNN1B missense mutation in a Chinese family with a history of stroke, and to confirm that the identified mutation is responsible for LS in this family. Methods: DNA samples were collected from the proband and 11 additional relatives. Next-generation sequencing was performed in the proband to find candidate variants. In order to exclude genetic polymorphism, the candidate variant in SCNN1B was verified in other family members, 100 hypertensives, and 100 healthy controls by Sanger sequencing. Results: Genetic testing revealed a novel and rare heterozygous variant in SCNN1B in the proband. This variant resulted in a substitution of threonine instead of proline at codon 617, altering the PY motif of β-ENaC. The identified mutation was only verified in 5 relatives. In silico analyses indicated that this variant was highly pathogenic. In this family, phenotypic heterogeneity was present among 6 LS patients. Tailored medicine with amiloride was effective in controlling hypertension and improving the

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Genetic Programming of Hypertension

Cited by 31 publications

References 103 publications

The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease

The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease

Control of blood pressure and cardiovascular outcomes in type 2 diabetes

Premature Stroke Secondary to Severe Hypertension Results from Liddle Syndrome Caused by a Novel SCNN1B Mutation

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