Evidence map›Paper›PMID 35426759›Full record

ArticleExpert opinion on therapeutic targets2022

Targeting calcium-mediated inter-organellar crosstalk in cardiac diseases.

Mohit M Hulsurkar, Satadru K Lahiri, Jason Karch, Meng C Wang, Xander H T Wehrens

Open access · greenAbstract read
In one paragraph

Article in Expert opinion on therapeutic targets, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. The Dysfunction of CaInternational journal of molecular sciences · 2023
    Review
  12. Review
  13. Role of CaArchives of toxicology · 2023
    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

5 authors at 2 institutions in 1 country.

Mohit M HulsurkarBaylor College of Medicine, Houston TX USA.ORCID 0000-0003-0595-6661
Satadru K LahiriBaylor College of Medicine, Houston TX USA.ORCID 0000-0001-9502-1530
Jason KarchBaylor College of Medicine, Houston TX USA.ORCID 0000-0002-3023-7469
Meng C WangBaylor College of Medicine, Houston TX USA.ORCID 0000-0002-5898-6007
Xander H T WehrensBaylor College of Medicine, Houston TX USA.ORCID 0000-0001-5044-672X
Baylor College of Medicine · USHoward Hughes Medical Institute · US

Funding

TMEM106b as a lysosomal adaptor to influence brain aging and tau pathogenesisP01AG066606 · NIA · BAYLOR COLLEGE OF MEDICINE · PI LI, FENG · 2021 to 2025
$13.5M
Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5M
Decode the chemical language that orchestrates cellular and organismal homeostasisDP1DK113644 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI WANG, MENG CARLA · 2016 to 2020
$5.5M
Targeting a lipid-mediated pro-longevity pathway as Alzheimer's therapyRF1AG062257 · NIA · BAYLOR COLLEGE OF MEDICINE · PI WANG, JIN, WANG, MENG CARLA · 2018 to 2020
$4.0M
Molecular Regulation of Mitochondrial Permeability Transition and its Role in Regulated NecrosisR01HL150031 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Jason Michael Karch · 2020 to 2026
$2.9M
Prebiotic Regulation of LongevityR01AT009050 · NCCIH · BAYLOR COLLEGE OF MEDICINE · PI WANG, MENG CARLA · 2016 to 2020
$2.6M
Junctophilin-2 cleavage in ischemic heart diseaseR01HL153350 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2021 to 2024
$2.3M
Mechanisms underlying atrial fibrillation associated with chronic kidney diseaseR01HL147108 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LI, NA, WEHRENS, XANDER H.T. · 2019 to 2022
$2.0M
LIPID SIGNALING IN REGULATION OF LONGEVITYR01AG045183 · NIA · BAYLOR COLLEGE OF MEDICINE · PI WANG, MENG CARLA · 2013 to 2017
$1.8M
Howard Hughes Medical InstituteNCCIH NIH HHS R01 AT009050NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL147108NHLBI NIH HHS R01 HL150031NHLBI NIH HHS R01 HL153350NIA NIH HHS P01 AG066606NIA NIH HHS R01 AG045183NIA NIH HHS RF1 AG062257NIDDK NIH HHS DP1 DK113644
6 · The paper itself

Abstract

introductionAbnormal calcium signaling between organelles such as the sarcoplasmic reticulum (SR), mitochondria and lysosomes is a key feature of heart diseases. Calcium serves as a secondary messenger mediating inter-organellar crosstalk, essential for maintaining the cardiomyocyte function. AREAS COVERED: This article examines the available literature related to calcium channels and transporters involved in inter-organellar calcium signaling. The SR calcium-release channels ryanodine receptor type-2 (RyR2) and inositol 1,4,5-trisphosphate receptor (IP EXPERT OPINION: Enhanced SR calcium release via RyR2 and reduced SR reuptake via SERCA2a, increased VDAC and MCUC-mediated calcium uptake into mitochondria, and enhanced lysosomal calcium-release via lysosomal TPC and TRPML may all contribute to aberrant calcium homeostasis causing heart disease. While mechanisms of this crosstalk need to be studied further, interventions targeting these calcium channels or combinations thereof might represent a promising therapeutic strategy.

Indexed as

Heart DiseasesRyanodine Receptor Calcium Release ChannelCalciumCalcium SignalingHumansMyocytes, CardiacSarcoplasmic ReticulumCalciumRyanodine Receptor Calcium Release ChannelCalciumCardiac Diseaseslysosomesmitochondriaorganelleryanodine receptorsarcoplasmic reticulum (SR)

Identifiers

PMID35426759
PMCPMC9081256
OpenAlexW4224037194

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.