Evidence map›Paper›PMID 27760997›Full record

ReviewHypertension research : official journal of the Japanese Society of Hypertension2017

Mineralocorticoid receptor as a therapeutic target in chronic kidney disease and hypertension.

Shigeru Shibata, Kenichi Ishizawa, Shunya Uchida

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Hypertension research : official journal of the Japanese Society of Hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Integrated morphological and transcriptomic analysis of bone disorders in aldosterone-salt hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  3. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Glomerular pressure and tubular oxygen supply: a critical dual target for renal protection.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Impact of mineralocorticoid receptor blockade with direct renin inhibition in angiotensin II-dependent hypertensive mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Article
  19. Recent advances in the management of secondary hypertension: chronic kidney disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
  20. Management of primary aldosteronism and mineralocorticoid receptor-associated hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
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 2 institutions in 1 country.

Shigeru ShibataDepartment of Internal Medicine, Division of Nephrology, Teikyo University School of Medicine, Tokyo, Japan.
Kenichi IshizawaDepartment of Internal Medicine, Division of Nephrology, Teikyo University School of Medicine, Tokyo, Japan.
Shunya UchidaDepartment of Internal Medicine, Division of Nephrology, Teikyo University School of Medicine, Tokyo, Japan.
Teikyo University · JPTokyo University of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidney has a central role in long-term control of blood pressure, and decreased kidney function is a common but difficult-to-treat cause of hypertension. Conversely, elevated blood pressure contributes to the progression of chronic kidney disease. Steroid hormone aldosterone and its receptor mineralocorticoid receptor (MR) contribute to hypertension by increasing renal salt reabsorption and promote kidney dysfunction through direct effects on renal parenchymal cells. Accumulating data indicate that various mechanisms affect aldosterone-MR signaling. Using a genetically engineered mouse model, we identified crosstalk between small GTPase Rac1 and MR. This crosstalk pathway promotes glomerular podocyte injury, and is also involved in the pathogenesis of hypertension. Notably, salt loading increases renal Rac1 activity in several models of salt-sensitive hypertension, which, in the presence of aldosterone, synergistically activates MR signaling, causing hypertension and kidney injury. There is also a mechanism regulating MR in a cell-selective manner. In the principal cells of the collecting duct, aldosterone directly binds and activate MR. In neighboring intercalated cells, however, binding of aldosterone to MR is regulated by phosphorylation at the ligand-binding domain. This mechanism serves as a switch to turn on electrolyte flux pathways in intercalated cells, allowing aldosterone to exert distinct effects in different physiological contexts. Given the potential benefit of MR blockade in hypertensive kidney disease, the delineation of these pathways may lead to the identification of alternative therapeutic targets. In this review, we discuss the roles of MR in mediating kidney disease and hypertension, with a focus on the crosstalk among related signaling pathways.

Indexed as

AnimalsHumansHypertensionMiceReceptors, MineralocorticoidRenal Insufficiency, ChronicSignal TransductionReceptors, Mineralocorticoid

Identifiers

PMID27760997
OpenAlexW2535727175

What OpenQuestion holds

Textmetadata
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.