Evidence map›Paper›PMID 12379817›Full record

ReviewHeart failure reviews2002

Regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis.

Kai C Wollert, Helmut Drexler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 102 citations in OpenAlex.

  1. Geraniin attenuates isoproterenol-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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  5. Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023
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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

2 authors at 1 institution in 1 country.

Kai C WollertDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany. wollert.kai@mh-hannover.de
Helmut Drexler
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy occurs in pathological conditions associated with chronic increases in hemodynamic load. Although hypertrophy can initially be viewed as a salutary response, ultimately, it often enters a phase of pathological remodeling that may lead to heart failure and premature death. A prevailing concept predicts that changes in gene expression in hypertrophied cardiac myocytes and cardiac myocyte loss by apoptosis contribute to the transition from hypertrophy to failure. In recent years, nitric oxide (NO) has emerged as an important regulator of cardiac remodeling. Specifically, NO has been recognized as a potent antihypertrophic and proapoptotic mediator in cultured cardiac myocytes. Studies in genetically engineered mice have extended these findings to the in vivo situation. It appears that low levels and transient release of NO by endothelial NO synthase exert beneficial effects on the remodeling process by reducing cardiac myocyte hypertrophy, cavity dilation and mortality. By contrast, high levels and sustained production of NO by inducible NO synthase seem to be maladaptive by reducing ventricular contractile function, and increasing cardiac myocyte apoptosis, and mortality. In the future, these novel insights into the role of NO in cardiac remodeling should allow the development of novel therapeutic strategies to treat cardiac remodeling and failure.

Indexed as

AnimalsApoptosisHeart FailureHumansHypertrophy, Left VentricularMiceNitric OxideNitric Oxide SynthaseVentricular RemodelingNitric OxideNitric Oxide Synthase

Identifiers

PMID12379817
OpenAlexW1521832143

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.