Evidence map›Paper›PMID 26775029›Full record

ReviewBiochimica et biophysica acta2016

Chronic heart failure: Ca(2+), catabolism, and catastrophic cell death.

Geoffrey W Cho, Francisco Altamirano, Joseph A Hill

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Heart Failure and Osteoporosis: Shared Challenges in the Aging Population.Journal of cardiovascular development and disease · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. International journal of molecular sciences · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

3 authors.

Geoffrey W ChoDepartment of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Francisco AltamiranoDepartment of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Joseph A HillDepartment of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: joseph.hill@utsouthwestern.edu.

Funding

Microenvironmental control of progenitors in organ dysfunction and repairU01HL100401 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N, SCHNEIDER, JAY W · 2009 to 2015
$8.3M
TRAINING PROGRAM IN LUNG BIOLOGY AND DISEASET32HL098040 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAUL, PHILIP W, TERADA, LANCE S · 2009 to 2024
$4.6M
FoxO-dependent Control of Cardiovascular RemodelingR01HL126012 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2016 to 2019
$1.6M
STIM1: Master Regulator of Calcium Homeostasis in CardiomyocytesR01HL120732 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL120732NHLBI NIH HHS R01 HL126012NHLBI NIH HHS T32 HL098040NHLBI NIH HHS U01 HL100401
6 · The paper itself

Abstract

Robust successes have been achieved in recent years in conquering the acutely lethal manifestations of heart disease. Many patients who previously would have died now survive to enjoy happy and productive lives. Nevertheless, the devastating impact of heart disease continues unabated, as the spectrum of disease has evolved with new manifestations. In light of this ever-evolving challenge, insights that culminate in novel therapeutic targets are urgently needed. Here, we review fundamental mechanisms of heart failure, both with reduced (HFrEF) and preserved (HFpEF) ejection fraction. We discuss pathways that regulate cardiomyocyte remodeling and turnover, focusing on Ca(2+) signaling, autophagy, and apoptosis. In particular, we highlight recent insights pointing to novel connections among these events. We also explore mechanisms whereby potential therapeutic approaches targeting these processes may improve morbidity and mortality in the devastating syndrome of heart failure.

Indexed as

Calcium SignalingAnimalsCalciumChronic DiseaseHeart FailureHumansMyocytes, CardiacCalciumApoptosisAutophagyCalcium homeostasisHeart failureRemodeling

Identifiers

PMID26775029
PMCPMC4791054

What OpenQuestion holds

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Registered trials

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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.