Evidence map›Paper›PMID 20823713›Full record

ReviewJournal of hypertension2010

Fibrosis in hypertensive heart disease: molecular pathways and cardioprotective strategies.

Atta U Shahbaz, Yao Sun, Syamal K Bhattacharya, Robert A Ahokas, Ivan C Gerling, Jesse E McGee, Karl T Weber

Open access · greenAbstract readReview
In one paragraph

Review in Journal of hypertension, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Myocardial Strain Imaging in Resistant Hypertension.Current hypertension reports · 2021
    Review
  9. The 3' Untranslated Region Protects the Heart from Angiotensin II-Induced Cardiac Dysfunction via AGGF1 Expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  10. Experimental Rodent Models of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2020
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Atta U ShahbazUniversity of Tennessee Health Science Center, 956 Court Ave., Memphis, TN 38163, USA.
Yao Sun
Syamal K Bhattacharya
Robert A Ahokas
Ivan C Gerling
Jesse E McGee
Karl T Weber
University of Tennessee Health Science Center · US

Funding

Aldosteronism: An Immunostimulatory StateR01HL073043 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WEBER, KARL T · 2004 to 2008
$1.8M
Recovery from Cachexia in Heart and Skeletal MuscleR01HL090867 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WEBER, KARL T · 2008 to 2011
$1.5M
Regulatory Mechanisms of Oxidative Stress in Hypertensive Heart DiseaseR01HL096813 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WEBER, KARL T · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL073043NHLBI NIH HHS R01 HL090867NHLBI NIH HHS R01 HL096813NHLBI NIH HHS R01-HL73043NHLBI NIH HHS R01-HL90867
6 · The paper itself

Abstract

Fibrosis is a fundamental component of the adverse structural remodelling of myocardium found in hypertensive heart disease (HHD). A replacement fibrosis appears at sites of previous cardiomyocyte necrosis to preserve the structural integrity of the myocardium. Such scarring has adverse functional consequences. The extensive distribution of fibrosis involving the right and left heart suggests cardiomyocyte necrosis is widespread. Together, the loss of these contractile elements and fibrous tissue deposition in the form of stiff in-series and in-parallel elastic elements contribute to the progressive failure of this normally efficient muscular pump. Pathogenic mechanisms modulating fibrous tissue formation at sites of repair include auto/paracrine properties of locally generated angiotensin II and endothelin-1. This study focuses on the signal-transducer-effector pathway involved in cardiomyocyte necrosis and the crucial pathogenic role of intracellular calcium overloading, and the subsequent induction of oxidative stress originating within its mitochondria that dictates the opening of the mitochondrial permeability transition pore. The ensuing osmotic destruction of these organelles is followed by necrotic cell death. It is now further recognized that calcium overloading of cardiac myocytes and mitochondria functioning as pro-oxidant is pathophysiologically counterbalanced by an intrinsically coupled zinc entry, which serves as an antioxidant. The prospect of raising intracellular zinc by adjuvant nutriceutical supplementation can, therefore, be preferentially exploited to uncouple this intrinsically coupled calcium-zinc dyshomeostasis in favour of endogenous antioxidant defences. Novel cardioprotective strategies may thus be at hand and deserve to be explored further in the overall management of patients with HHD.

Indexed as

FibrosisAnimalsAntioxidantsBlack PeopleCardiotonic AgentsDisease Models, AnimalHeart DiseasesHumansHypertensionMaleRatsRats, Sprague-DawleyReninAntioxidantsCardiotonic AgentsRenin

Identifiers

PMID20823713
PMCPMC2992441
OpenAlexW2026789574

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.