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Updated: Jun 25, 2025

Analysis of Tubular Membrane Networks in Cardiac Myocytes from Atria and Ventricles
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FGF13 deficiency ameliorates calcium signaling abnormality in heart failure by regulating microtubule stability

Ran Zhao1, Yingke Yan1, Yiming Dong1

  • 1Department of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, The Hebei Collaboration Innovation Center for Mechanism, Diagnosis and Treatment of Neurological and Psychiatric Disease, Hebei Medical University, Shijiazhuang 050017, China.

Biochemical Pharmacology
|May 31, 2024
PubMed

Insights

Fibroblast growth factor 13 (FGF13) deficiency improves heart failure by normalizing calcium signaling. This occurs by inhibiting increased microtubule stability, offering new therapeutic targets for heart failure.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Physiology

Background:

  • Calcium signaling abnormalities in cardiomyocytes are central to heart failure development.
  • Fibroblast growth factor 13 (FGF13) has known cardiac regulatory roles, but its involvement in heart failure-related calcium handling is unclear.

Purpose of the Study:

  • To investigate the role and mechanism of FGF13 in cardiac calcium mishandling during heart failure.
  • To determine if FGF13 influences microtubule stability in the failing heart.

Main Methods:

  • A mouse model of heart failure was created using transaortic constriction.
  • Cardiac function, calcium transients, Cav1.2 and Serca2α expression/activity were assessed.
  • Microtubule stability was analyzed in vivo and in vitro using FGF13 knockdown and overexpression in neonatal rat ventricular myocytes (NRVMs).

Main Results:

  • FGF13 deficiency alleviated cardiac dysfunction and normalized calcium transients in heart failure mice.
  • FGF13 deficiency restored Cav1.2 and Serca2α expression and activity.
  • FGF13 deficiency inhibited the increased microtubule stability observed in heart failure, and FGF13's microtubule-binding ability was crucial for its detrimental effects on calcium handling.

Conclusions:

  • FGF13 deficiency improves cardiac calcium signaling in heart failure by inhibiting increased microtubule stability.
  • FGF13 plays a critical role in cardiac calcium homeostasis and presents a potential therapeutic target for heart failure prevention and treatment.
Keywords:
Calcium signallingCalcium transientsFibroblast growth factor 13Heart failureL-type calcium channelMicrotubules

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