Evidence map›Paper›PMID 22258323›Full record

ReviewKidney international2012

Synthesis and secretion of renin in mice with induced genetic mutations.

Jurgen Schnermann, Josephine P Briggs

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Non-Hypertensive Effects of Aldosterone.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Endocrine functions of the renal interstitium.Pflugers Archiv : European journal of physiology · 2017
    Review
  11. Physiology and Pathophysiology of the Intrarenal Renin-Angiotensin System: An Update.Journal of the American Society of Nephrology : JASN · 2017
    Review
  12. Article
  13. Newly stemming functions of macula densa-derived prostanoids.Hypertension (Dallas, Tex. : 1979) · 2015
    Article
  14. AMPK couples plasma renin to cellular metabolism by phosphorylation of ACC1.American journal of physiology. Renal physiology · 2013
    Article
  15. Article
  16. Metabolic control of renin secretion.Pflugers Archiv : European journal of physiology · 2013
    Review
  17. Renal renin secretion as regulator of body fluid homeostasis.Pflugers Archiv : European journal of physiology · 2013
    Review
  18. 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

2 authors at 1 institution in 1 country.

Jurgen SchnermannNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. jurgens@intra.niddk.nih.gov
Josephine P Briggs
National Institutes of Health · US

Funding

Renal Function In Transgenic MiceZIADK043408 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SCHNERMANN, JURGEN · 2009 to 2012
$3.7M
Intramural NIH HHS ZIA DK043408
6 · The paper itself

Abstract

The juxtaglomerular (JG) cell product renin is rate limiting in the generation of the bioactive octapeptide angiotensin II. Rates of synthesis and secretion of the aspartyl protease renin by JG cells are controlled by multiple afferent and efferent pathways originating in the CNS, cardiovascular system, and kidneys, and making critical contributions to the maintenance of extracellular fluid volume and arterial blood pressure. Since both excesses and deficits of angiotensin II have deleterious effects, it is not surprising that control of renin is secured by a complex system of feedforward and feedback relationships. Mice with genetic alterations have contributed to a better understanding of the networks controlling renin synthesis and secretion. Essential input for the setting of basal renin generation rates is provided by β-adrenergic receptors acting through cyclic adenosine monophosphate, the primary intracellular activation mechanism for renin mRNA generation. Other major control mechanisms include COX-2 and nNOS affecting renin through PGE2, PGI2, and nitric oxide. Angiotensin II provides strong negative feedback inhibition of renin synthesis, largely an indirect effect mediated by baroreceptor and macula densa inputs. Adenosine appears to be a dominant factor in the inhibitory arms of the baroreceptor and macula densa mechanisms. Targeted gene mutations have also shed light on a number of novel aspects related to renin processing and the regulation of renin synthesis and secretion.

Indexed as

MutationAnimalsAnimals, Genetically ModifiedConnexinsFeedback, PhysiologicalGene Expression RegulationGenotypeJuxtaglomerular ApparatusMiceNitric Oxide SynthasePhenotypeProstaglandin-Endoperoxide SynthasesReceptors, AdrenergicReceptors, ProstaglandinReceptors, Purinergic P1ReninConnexinsNitric Oxide SynthaseProstaglandin-Endoperoxide SynthasesReceptors, AdrenergicReceptors, ProstaglandinReceptors, Purinergic P1Renin

Identifiers

PMID22258323
PMCPMC3482822
OpenAlexW2086813947

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.