Evidence map›Paper›PMID 29463624›Full record

ArticleHypertension (Dallas, Tex. : 1979)2018

Smooth Muscle Cell-Mineralocorticoid Receptor as a Mediator of Cardiovascular Stiffness With Aging.

Seung Kyum Kim, Amy T McCurley, Jennifer J DuPont, Mark Aronovitz, M Elizabeth Moss, Isaac E Stillman, S Ananth Karumanchi, Demetra D Christou, Iris Z Jaffe

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  6. Article
  7. The angiotensin II type 2 receptor attenuates aging-associated arterial stiffness in female mice.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Resistant Hypertension: A Brief Review of Pathophysiology.Journal of general internal medicine · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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  18. Review
  19. Review
  20. Primary hyperaldosteronism in Acute Central Serous Chorioretinopathy: a real need for screening?Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    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

9 authors at 2 institutions in 1 country.

Seung Kyum KimFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Amy T McCurleyFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Jennifer J DuPontFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Mark AronovitzFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
M Elizabeth MossFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Isaac E StillmanFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
S Ananth KarumanchiFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Demetra D ChristouFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.).
Iris Z JaffeFrom the Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (S.K.K., A.T.M., J.J.D., M.A., M.E.M., I.Z.J.); Departments of Pathology (I.E.S.) and Medicine and Obstetrics and Gynecology (S.A.K.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; and Department of Applied Physiology and Kinesiology, University of Florida, Gainesville (D.D.C.). ijaffe@tuftsmedicalcenter.org.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

Boston University Clinical and Translational Science Award (CTSA) Program UL1UL1TR000157 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2012 to 2013
$7.9M
The Role of Vascular MR-Regulated Genes in Vascular Function and DiseaseR01HL095590 · NHLBI · TUFTS MEDICAL CENTER · PI Iris Z Jaffe · 2009 to 2026
$7.7M
Smooth Muscle Mineralocorticoid Receptors in Vascular Aging and HypertensionR01HL119290 · NHLBI · TUFTS MEDICAL CENTER · PI Iris Z Jaffe · 2014 to 2026
$7.0M
Tufts BIRCWH ProgramK12HD092535 · NICHD · TUFTS UNIVERSITY BOSTON · PI FREUND, KAREN, JAFFE, IRIS Z · 2017 to 2023
$4.3M
The Role of Endothelial Cell Mineralocorticoid Receptors in the Development of Vascular Inflammation and AtherosclerosisF30HL137255 · NHLBI · TUFTS UNIVERSITY BOSTON · PI MOSS, MARY ELIZABETH · 2017 to 2021
$184k
Endothelial Dysfunction in Older Adult Humans with the Metabolic SyndromeR03AG032067 · NIA · UNIVERSITY OF FLORIDA · PI CHRISTOU, DEMETRA · 2008 to 2009
$125k
NCATS NIH HHS UL1 TR000157NHLBI NIH HHS F30 HL137255NHLBI NIH HHS R01 HL095590NHLBI NIH HHS R01 HL119290NIA NIH HHS R03 AG032067NICHD NIH HHS K12 HD092535
6 · The paper itself

Abstract

Stiffening of the vasculature with aging is a strong predictor of adverse cardiovascular events, independent of all other risk factors including blood pressure, yet no therapies target this process. MRs (mineralocorticoid receptors) in smooth muscle cells (SMCs) have been implicated in the regulation of vascular fibrosis but have not been explored in vascular aging. Comparing SMC-MR-deleted male mice to MR-intact littermates at 3, 12, and 18 months of age, we demonstrated that aging-associated vascular stiffening and fibrosis are mitigated by MR deletion in SMCs. Progression of cardiac stiffness and fibrosis and the decline in exercise capacity with aging were also mitigated by MR deletion in SMC. Vascular gene expression profiling analysis revealed that MR deletion in SMC is associated with recruitment of a distinct antifibrotic vascular gene expression program with aging. Moreover, long-term pharmacological inhibition of MR in aged mice prevented the progression of vascular fibrosis and stiffness and induced a similar antifibrotic vascular gene program. Finally, in a small trial in elderly male humans, short-term MR antagonism produced an antifibrotic signature of circulating biomarkers similar to that observed in the vasculature of SMC-MR-deleted mice. These findings suggest that SMC-MR contributes to vascular stiffening with aging and is a potential therapeutic target to prevent the progression of aging-associated vascular fibrosis and stiffness.

Indexed as

Cellular SenescenceMuscle, Smooth, VascularMyocytes, Smooth MuscleReceptors, MineralocorticoidSpironolactoneVascular StiffnessAgedAnimalsDisease ProgressionExercise ToleranceFibrosisGene ExpressionGene Expression ProfilingHumansMaleMiceMineralocorticoid Receptor AntagonistsReceptors, MineralocorticoidSpironolactoneblood pressuregene expression profilingmyocytes, smooth musclereceptors, mineralocorticoidvascular stiffening

Identifiers

PMID29463624
PMCPMC5843545
OpenAlexW2790443436

What OpenQuestion holds

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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.