Evidence map›Paper›PMID 31313674›Full record

ReviewCurrent opinion in nephrology and hypertension2019

Molecular regulation of NKCC2 in blood pressure control and hypertension.

Paulo S Caceres, Pablo A Ortiz

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. TNF inhibits NKCC2 phosphorylation by a calcineurin-dependent pathway.American journal of physiology. Renal physiology · 2025
    Article
  7. Article
  8. Uromodulin biology.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. The role of uromodulin in cardiovascular disease: a review.Frontiers in cardiovascular medicine · 2024
    Review
  13. Review
  14. Dopamine Receptor DThe Yale journal of biology and medicine · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Paulo S CaceresDepartment of Ophthalmology, Weill Cornell Medical College, Margaret Dyson Vision Research Institute, New York, New York.
Pablo A OrtizHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan, USA.
Cornell University · USHenry Ford Hospital · US

Funding

RETINA--REVERSED POLARITY IN RPER01EY008538 · NEI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RODRIGUEZ-BOULAN, ENRIQUE J · 1991 to 2020
$13.4M
Fructose induced salt-sensitive hypertension: Role of thick ascending limb transportR01DK107263 · NIDDK · HENRY FORD HEALTH SYSTEM · PI ORTIZ, PABLO A. · 2016 to 2020
$2.1M
NEI NIH HHS R01 EY008538NIDDK NIH HHS R01 DK107263
6 · The paper itself

Abstract

purpose of reviewThe apical Na/K/2Cl cotransporter (NKCC2) mediates NaCl reabsorption by the thick ascending limb, contributing to maintenance of blood pressure (BP). Despite effective NKCC2 inhibition by loop diuretics, these agents are not viable for long-term management of BP due to side effects. Novel molecular mechanisms that control NKCC2 activity reveal an increasingly complex picture with interacting layers of NKCC2 regulation. Here, we review the latest developments that shine new light on NKCC2-mediated control of BP and potential new long-term therapies to treat hypertension. RECENT

findingsEmerging molecular NKCC2 regulators, often binding partners, reveal a complex overlay of interacting mechanisms aimed at fine tuning NKCC2 activity. Different factors achieve this by shifting the balance between trafficking steps like exocytosis, endocytosis, recycling and protein turnover, or by balancing phosphorylation vs. dephosphorylation. Further molecular details are also emerging on previously known pathways of NKCC2 regulation, and recent in-vivo data continues to place NKCC2 regulation at the center of BP control. SUMMARY: Several layers of emerging molecular mechanisms that control NKCC2 activity may operate simultaneously, but they can also be controlled independently. This provides an opportunity to identify new pharmacological targets to fine-tune NKCC2 activity for BP management.

Indexed as

AnimalsAntigens, NeoplasmBlood PressureCell Cycle ProteinsHumansHypertensionNeoplasm ProteinsPhosphorylationProtein Serine-Threonine KinasesSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1ALMS1 protein, humanAntigens, NeoplasmCell Cycle ProteinsMAGED1 protein, humanNeoplasm ProteinsProtein Serine-Threonine KinasesSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1WNK4 protein, human

Identifiers

PMID31313674
PMCPMC7226929
OpenAlexW2957604817

What OpenQuestion holds

Textmetadata
LicenceTDM
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.