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Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...

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Related Experiment Video

Updated: May 14, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

KLF9 Aggravates Doxorubicin-Induced Cardiotoxicity by Regulating the ROS/p53 Signalling Pathway.

Jingfeng Peng1,2,3, Jianhua Wang2,3, Hui Feng2,3,4

  • 1Department of Cardiology, Nantong First People's Hospital, Nantong, 226000, Jiangsu, China.

Cardiovascular Toxicology
|May 13, 2026
PubMed
Summary
This summary is machine-generated.

Krüppel-like factor 9 (KLF9) exacerbates doxorubicin (DOX)-induced heart damage by promoting apoptosis. Silencing KLF9 protects against DOX cardiotoxicity by upregulating thioredoxin reductase 2 and modulating ROS/p53 signaling.

Keywords:
ApoptosisDoxorubicinKrüppel-like factor 9Myocardial injuryReactive oxygen species

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Last Updated: May 14, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Oncology

Background:

  • Doxorubicin (DOX) is a vital chemotherapy drug, but its use is limited by cardiotoxicity.
  • Krüppel-like factor 9 (KLF9) influences cell processes and cardiovascular health.

Purpose of the Study:

  • To investigate the role of KLF9 in doxorubicin-induced cardiotoxicity.
  • To elucidate the underlying molecular mechanisms of KLF9's effect on DOX cardiotoxicity.

Main Methods:

  • Established a mouse model of DOX-induced cardiotoxicity with cardiac-specific KLF9 overexpression or silencing.
  • Assessed cardiac function, myocardial injury, apoptosis, and key molecular pathways (Txnrd2, ROS, p53).
  • Validated findings in vitro using H9c2 cells.

Main Results:

  • KLF9 expression increased in DOX-treated hearts and cells.
  • KLF9 overexpression worsened DOX cardiotoxicity; KLF9 silencing alleviated it.
  • KLF9 deficiency upregulated Txnrd2, suppressed apoptosis via ROS/p53 signaling.

Conclusions:

  • KLF9 promotes DOX-induced cardiotoxicity by inhibiting Txnrd2 and modulating ROS/p53 signaling.
  • Targeting KLF9 may offer a strategy to mitigate DOX cardiotoxicity.