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Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
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Arrhythmias are disturbances in the heart's rhythm that lead to abnormal heartbeats. These irregularities can originate from different parts of the heart and are classified based on their origin and nature.
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Residue-Specific Exchange of Proline by Proline Analogs in Fluorescent Proteins: How "Molecular Surgery" of the Backbone Affects Folding and Stability
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Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism.

Hangying Ying1,2,3, Hangping Fan4,5, Yunhe Wang1

  • 1Department of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 31, 2026
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Summary

Reduced connexin43 (Cx43) causes life-threatening ventricular arrhythmias (VAs). Cx43 deficiency impairs proline metabolism via SNAT2, leading to mitochondrial dysfunction and arrhythmias. Proline supplementation rescues this phenotype.

Keywords:
ROSconnexin43iPSC‐CMsprolineventricular arrhythmias

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Metabolic Research

Background:

  • Ventricular arrhythmias (VAs) are critical heart rhythm disorders.
  • Reduced connexin43 (Cx43) is implicated in VA mechanisms.
  • The precise molecular link between Cx43 downregulation and VA development is not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanism connecting Cx43 deficiency to VA formation.
  • To investigate the role of proline metabolism in Cx43-related arrhythmias.
  • To explore potential therapeutic strategies targeting proline metabolism for VAs.

Main Methods:

  • Utilized Cx43 knockout (Cx43-KO) induced pluripotent stem-derived cardiomyocytes.
  • Employed cardiac-specific conditional Cx43-KO (Cx43-cKO) mice models.
  • Assessed proline levels, SNAT2 expression, mitochondrial function, and calcium handling.

Main Results:

  • Cx43 deficiency induced an arrhythmic phenotype and decreased proline content in vitro and in vivo.
  • Cx43 interacts with SNAT2, and its deficiency impairs proline transport and metabolism.
  • This metabolic disruption caused mitochondrial dysfunction, oxidative stress, and abnormal calcium handling, leading to arrhythmias.
  • Exogenous proline supplementation restored metabolic balance and rescued the arrhythmic phenotype in Cx43-cKO mice.

Conclusions:

  • Cx43 deficiency triggers VAs via SNAT2-mediated proline metabolic reprogramming.
  • Disruption of proline metabolism is a key mechanism underlying Cx43-associated arrhythmias.
  • Targeting proline metabolism presents a novel therapeutic avenue for treating VAs.