Evidence map›Paper›PMID 27306796›Full record

ReviewCurrent opinion in nephrology and hypertension2016

Basolateral Kir4.1 activity in the distal convoluted tubule regulates K secretion by determining NaCl cotransporter activity.

Wen-Hui Wang

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
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

1 author at 1 institution in 1 country.

Wen-Hui WangDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
New York Medical College · US

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI JIANG, HOULI · 1985 to 2015
$33.4M
Role of Kir4.1 in Regulating NCC and ROMK in DCTR01DK054983 · NIDDK · NEW YORK MEDICAL COLLEGE · PI ELLISON, DAVID H, WANG, WENHUI · 2001 to 2020
$7.4M
Role of Kir4.1 in Regulating NCC and ROMK in DCTR56DK054983 · NIDDK · NEW YORK MEDICAL COLLEGE · PI ELLISON, DAVID H, WANG, WENHUI · 2021 to 2021
$100k
NHLBI NIH HHS P01 HL034300NIDDK NIH HHS R01 DK054983NIDDK NIH HHS R56 DK054983
6 · The paper itself

Abstract

purpose of reviewRenal potassium (K) secretion plays a key role in maintaining K homeostasis. The classic mechanism of renal K secretion is focused on the connecting tubule and cortical collecting duct, in which K is uptaken by basolateral Na-K-ATPase and is secreted into the lumen by apical ROMK (Kir1.1) and Ca-activated big conductance K channel. Recently, genetic studies and animal models have indicated that inwardly rectifying K channel 4.1 (Kir4.1 or Kcnj10) in the distal convoluted tubule (DCT) may play a role in the regulation of K secretion in the aldosterone-sensitive distal nephron by targeting the NaCl cotransporter (NCC). This review summarizes recent progresses regarding the role of Kir4.1 in the regulation of NCC and K secretion. RECENT

findingsKir4.1 is expressed in the basolateral membrane of the DCT, and plays a predominant role in contributing to the basolateral K conductance and in participating in the generation of negative membrane potential. Kir4.1 is also the substrate of src-family tyrosine kinase and the stimulation of src-family tyrosine kinase activates Kir4.1 activity in the DCT. The genetic deletion or functional inhibition of Kir4.1 depolarizes the membrane of the DCT, inhibits ste20-proline-alanine rich kinase, and suppresses NCC activity. Moreover, the downregulation of Kir4.1 increases epithelial Na channel expression in the collecting duct and urinary K excretion. Finally, mice with low Kir4.1 activity in the DCT are hypomagnesemia and hypokalemia. SUMMARY: Recent progress in exploring the regulation and the function of Kir4.1 in the DCT strongly indicates that Kir4.1plays an important role in initiating the regulation of renal K secretion by targeting NCC and it may serves as a K sensor in the kidney.

Indexed as

AnimalsCell MembraneHumansIon TransportKcnj10 ChannelKidney Tubules, DistalMembrane PotentialsPotassiumPotassium Channels, Inwardly RectifyingSolute Carrier Family 12, Member 3Kcnj10 ChannelPotassiumPotassium Channels, Inwardly RectifyingSolute Carrier Family 12, Member 3

Identifiers

PMID27306796
PMCPMC4974141
OpenAlexW2436311192

What OpenQuestion holds

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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.