Evidence map›Paper›PMID 32852625›Full record

ReviewCurrent hypertension reports2020

Cullin-3: Renal and Vascular Mechanisms Regulating Blood Pressure.

Jing Wu, James A McCormick, Curt D Sigmund

Open access · greenAbstract readReview
In one paragraph

Review in Current hypertension reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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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 2 institutions in 1 country.

Jing WuDepartment of Physiology, Cardiovascular Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226-0509, USA.
James A McCormickDivision of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR, 97239, USA.
Curt D SigmundDepartment of Physiology, Cardiovascular Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226-0509, USA. csigmund@mcw.edu.
Medical College of Wisconsin · USOregon Health & Science University · US

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI GROBE, JUSTIN L · 2007 to 2022
$30.2M
PPARG-dependent Mechanisms Control Endothelial-Smooth Muscle Coordination, Arterial Pressure, Vasomotor Function and Arterial StiffnessR35HL144807 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI SIGMUND, CURT DANIEL · 2019 to 2024
$5.5M
Regulation of sodium transport and blood pressure by SPAK/OSR1 kinasesR01DK098141 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI JAMES A MCCORMICK, Ujwal Shinde · 2014 to 2026
$4.2M
Regulation of renal ion transport by the CUL3-WNK-SPAK pathwayR56DK117903 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI MCCORMICK, JAMES A · 2019 to 2019
$116k
NHLBI NIH HHS P01 HL084207NHLBI NIH HHS R35 HL144807NIDDK NIH HHS R01 DK098141NIDDK NIH HHS R56 DK117903
6 · The paper itself

Abstract

purpose of reviewThe goal of this review is to evaluate recent advances in understanding the pivotal roles of Cullin-3 (CUL3) in blood pressure regulation with a focus on its actions in the kidney and blood vessels. RECENT

findingsCul3-based ubiquitin ligase regulates renal electrolyte transport, vascular tone, and redox homeostasis by facilitating the normal turnover of (1) with-no-lysine kinases in the distal nephron, (2) RhoA and phosphodiesterase 5 in the vascular smooth muscle, and (3) nuclear factor E2-related factor 2 in antioxidant responses. CUL3 mutations identified in familial hyperkalemic hypertension (FHHt) yield a mutant protein lacking exon 9 (CUL3∆9) which displays dual gain and loss of function. CUL3∆9 acts in a dominant manner to impair CUL3-mediated substrate ubiquitylation and degradation. The consequent accumulation of substrates and overactivation of downstream signaling cause FHHt through increased sodium reabsorption, enhanced vasoconstriction, and decreased vasodilation. CUL3 ubiquitin ligase maintains normal cardiovascular and renal physiology through posttranslational modification of key substrates which regulate blood pressure. Interference with CUL3 disturbs these key downstream pathways. Further understanding the spatial and temporal specificity of how CUL3 functions in these pathways is necessary to identify novel therapeutic targets for hypertension.

Indexed as

Cullin ProteinsHypertensionBlood PressureHumansKidneyProtein Serine-Threonine KinasesCullin ProteinsProtein Serine-Threonine KinasesBlood pressureCullin3Phosphodiesterase 5RhoAUbiquitylationWith-no-lysine kinases

Identifiers

PMID32852625
PMCPMC7477742
OpenAlexW3080857438

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.