Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Lineage-restricted dependency on an oncofetal SNHG29-IGF2BP1 RNA axis in acute megakaryoblastic leukemia.

Leukemia·2026
Same author

Loss of erythrocyte arginase-1 impairs vasorelaxation due to endothelial GSNOR overexpression and denitrosylation of G protein subunits.

Redox biology·2026
Same author

The conjugation-resistant bile acid norUDCA cures liver fibrosis but impairs systemic energy metabolism.

Molecular metabolism·2026
Same author

LINC00607 facilitates endothelial VEGF-A receptor FLT1 splicing.

Molecular therapy : the journal of the American Society of Gene Therapy·2026
Same author

Higher sensitivity to ouabain-induced toxicity in human induced pluripotent stem cell-derived cardiomyocytes than human adult heart tissue despite similar Na<sup>+</sup>/K<sup>+</sup>-ATPase pump current amplitudes.

British journal of pharmacology·2026
Same author

Generation of human induced pluripotent stem cell lines carrying a heterozygous and homozygous PRKD1 c.1774G > A genetic variant causing syndromic congenital defects.

Stem cell research·2026
Same journal

Corrigendum to: "NO modulates human airway smooth muscle function by altering glucose-6-phosphate dehydrogenase effects on sGC function in asthma" [Redox Biology 95 (2026) 104262].

Redox biology·2026
Same journal

Inhibiting 15-PGDH restores redox homeostasis and confers neuroprotection in Parkinson's disease.

Redox biology·2026
Same journal

Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.

Redox biology·2026
Same journal

Glutathione metabolism-linked ferroptosis in human seminoma: a spatial multi-omics mapping study.

Redox biology·2026
Same journal

Apurinic/apyrimidinic endonuclease 1 prevents oxidative DNA damage in intestinal epithelial cells induced by genotoxic Escherichia coli NC101.

Redox biology·2026
Same journal

Low serum selenium combined with SELENOP-autoantibodies are associated with persistent fatigue after SARS-CoV-2 infection.

Redox biology·2026
See all related articles

Related Experiment Video

Updated: Nov 9, 2025

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology
10:41

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Published on: January 23, 2021

8.0K

Sulforaphane exposure impairs contractility and mitochondrial function in three-dimensional engineered heart tissue.

Alexandra Rhoden1, Felix W Friedrich1, Theresa Brandt2

  • 1Institute of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.

Redox Biology
|April 8, 2021
PubMed
Summary
This summary is machine-generated.

Sulforaphane (SFN) negatively impacts heart contractility by causing mitochondrial dysfunction. This research highlights potential cardiac risks associated with SFN supplementation, especially in patients with existing cardiovascular conditions.

Keywords:
Contractile and mitochondrial functionEngineered heart tissueSulforaphane

More Related Videos

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues
08:07

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Published on: April 7, 2023

3.9K
Fabrication of 3D Cardiac Microtissue Arrays using Human iPSC-Derived Cardiomyocytes, Cardiac Fibroblasts, and Endothelial Cells
10:37

Fabrication of 3D Cardiac Microtissue Arrays using Human iPSC-Derived Cardiomyocytes, Cardiac Fibroblasts, and Endothelial Cells

Published on: March 14, 2021

6.9K

Related Experiment Videos

Last Updated: Nov 9, 2025

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology
10:41

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Published on: January 23, 2021

8.0K
Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues
08:07

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Published on: April 7, 2023

3.9K
Fabrication of 3D Cardiac Microtissue Arrays using Human iPSC-Derived Cardiomyocytes, Cardiac Fibroblasts, and Endothelial Cells
10:37

Fabrication of 3D Cardiac Microtissue Arrays using Human iPSC-Derived Cardiomyocytes, Cardiac Fibroblasts, and Endothelial Cells

Published on: March 14, 2021

6.9K

Area of Science:

  • Biochemistry
  • Cardiology
  • Pharmacology

Background:

  • Sulforaphane (SFN), a cruciferous plant phytochemical, has therapeutic potential for neurological disorders and cancer.
  • SFN's reactivity allows protein modification, influencing cellular functions.
  • Potential cardiac side effects of SFN remain largely uninvestigated.

Purpose of the Study:

  • To investigate the impact of Sulforaphane on cardiomyocyte contractile function.
  • To characterize the cellular mechanisms underlying SFN's effects on cardiac tissue.
  • To assess the safety of SFN supplementation concerning heart function.

Main Methods:

  • Studied SFN effects on cardiac preparations from neonatal rat, adult mouse, and human iPSC-derived cardiomyocytes.
  • Assessed cardiomyocyte contractility, Frank-Starling response, and myofilament function.
  • Utilized transmission electron microscopy and biochemical assays to evaluate mitochondrial function and cellular damage.

Main Results:

  • SFN induced a negative inotropic effect, impairing contractility and the Frank-Starling response.
  • Mitochondrial dysfunction was evident, with increased lactate, ROS production, and reduced membrane potential.
  • SFN exposure led to disturbed sarcomeric organization and altered mitochondrial morphology.

Conclusions:

  • SFN exerts a negative inotropic effect on cardiomyocytes, mediated by mitochondrial dysfunction.
  • Cardiac contractility may be compromised in patients with cardiovascular comorbidities undergoing SFN therapy.
  • Regular cardiac function monitoring is recommended to prevent potential SFN-induced cardiotoxicity.