Evidence map›Paper›PMID 34094823›Full record

ReviewActa pharmaceutica Sinica. B2021

Regulatory control of the Na-Cl co-transporter NCC and its therapeutic potential for hypertension.

Nur Farah Meor Azlan, Maarten P Koeners, Jinwei Zhang

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Diet-induced obesity impairs salt-dependent downregulation of NCC activity.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Nur Farah Meor AzlanInstitute of Biomedical and Clinical Sciences, Medical School, College of Medicine and Health, University of Exeter, Hatherly Laboratories, Exeter EX4 4PS, UK.
Maarten P KoenersInstitute of Biomedical and Clinical Sciences, Medical School, College of Medicine and Health, University of Exeter, Hatherly Laboratories, Exeter EX4 4PS, UK.
Jinwei ZhangInstitute of Biomedical and Clinical Sciences, Medical School, College of Medicine and Health, University of Exeter, Hatherly Laboratories, Exeter EX4 4PS, UK.
University of Exeter · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is the largest risk factor for cardiovascular disease, the leading cause of mortality worldwide. As blood pressure regulation is influenced by multiple physiological systems, hypertension cannot be attributed to a single identifiable etiology. Three decades of research into Mendelian forms of hypertension implicated alterations in the renal tubular sodium handling, particularly the distal convoluted tubule (DCT)-native, thiazide-sensitive Na-Cl cotransporter (NCC). Altered functions of the NCC have shown to have profound effects on blood pressure regulation as illustrated by the over activation and inactivation of the NCC in Gordon's and Gitelman syndromes respectively. Substantial progress has uncovered multiple factors that affect the expression and activity of the NCC. In particular, NCC activity is controlled by phosphorylation/dephosphorylation, and NCC expression is facilitated by glycosylation and negatively regulated by ubiquitination. Studies have even found parvalbumin to be an unexpected regulator of the NCC. In recent years, there have been considerable advances in our understanding of NCC control mechanisms, particularly

Indexed as

ATP, adenosine triphosphateBlood pressure regulationCa2+, calcium ionCardiovascular diseaseCCC, cation-coupled chloride cotransportersCCT, conserved carboxy-terminalCNI, calcineurin inhibitorsCUL3, cullin 3CUL3/KLHL3-WNK-SPAK/OSR1DAG, diacylglycerolDCT, distal convoluted tubuleDUSP, dual specificity phosphatasesECF, extracellular fluidELISA, enzyme-bound immunosorbent analysisEnaC, epithelial sodium channelsERK, extracellular signal-regulated kinasesGABA, gamma-aminobutyric acidHEK293, human embryonic kidney 293HypertensionI1, inhibitor 1KCC, potassium-chloride-cotransportersKinase inhibitorsKLHL3, kelch-like 3K+, potassium ionKS-WNK1, kidney specific-WNK1MAPK, mitogen-activated protein kinasemDCT, mammalian DCTMembrane traffickingMO25, mouse protein-25mRNA, messenger RNANaCl-cotransporter NCCNaCl, sodium chlorideNa+, sodium ionNCC, sodium–chloride cotransportersNKCC, sodium–potassium–chloride-cotransporterOSR1, oxidative stress-responsive gene 1PCT, proximal convoluted tubulePHAII, pseudohypoaldosteronism type IIPP, protein phosphatasePV, parvalbuminRasGRP1, RAS guanyl-releasing protein 1ROMK, renal outer medullary potassiumSLC12, solute carrier 12SPAK, Ste20-related proline-alanine-rich-kinaseTAL, thick ascending limbTherapeutic targetsWNK, with-no-lysine kinases

Identifiers

PMID34094823
PMCPMC8144889
OpenAlexW3088227706

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.