Metabolic Perturbation Exacerbates Sinoatrial Node Dysfunction in Heart Failure

Heart failure (HF) affects approximately 6.2 million people in the United States, with a 5-year mortality exceeding 50%. Bradyarrhythmia, a known complication in HF due to sinoatrial node (SAN) dysfunction (SAND), increases the morbidity and mortality of HF patients. Insights into the mechanistic underpinnings of SAND in HF could therefore uncover vital therapeutic targets to improve clinical outcomes. The SAN cells are endowed with a dense mitochondrial network crucial for sustaining their pacemaking function on a beat-to-beat basis. We have previously demonstrated significant disruptions in the mitochondrial-sarcoplasmic reticulum connectomics, resulting in abnormal mitochondrial Ca <sup>2+</sup> handling and impaired mitochondrial function in HF. Here, we hypothesize that the metabolic perturbation is one of the critical mechanisms underlying SAND. To this end, we took advantage of a multi-omics approach combined with ultra-resolution imaging and functional analyses to decipher the metabolic shift that transpires in the HF SAN. Our findings revealed significant metabolic remodeling within the SAN mitochondria in HF, with a diminished reliance on fatty acid β-oxidation, enhanced utilization of ketone bodies, and heightened dependence on carbohydrate catabolism. Notably, metabolomics analyses identified the pronounced increase of glucosylceramides and ceramides as one of the mechanisms leading to mitochondrial dysfunction. We directly test this hypothesis and demonstrate that ceramides induce a dose-dependent metabolic shift from oxidative phosphorylation to glycolysis. Importantly, these alterations lead to a significant impairment in SAN automaticity in a dose-dependent manner. Collectively, the findings support the notion that ceramides are not only markers of metabolic derangement, but also active mediators of mitochondrial and metabolic dysfunction in the SAN. Overall, the study provides evidence that ceramides may be a potential therapeutic target for mitigating SAND in HF.

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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-02-10
DOI
https://doi.org/10.64898/2026.02.06.704519
Primary Topic
Cardiovascular Function and Risk Factors
Type
article
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article

Metabolic Perturbation Exacerbates Sinoatrial Node Dysfunction in Heart Failure

Joe Z. Zhang, Nipavan Chiamvimonvat, Guy Perkins, Phung Ngoc Thai et al.
bioRxiv (Cold Spring Harbor Laboratory)
Cardiovascular Function and Risk Factors
article

Metabolic Perturbation Exacerbates Sinoatrial Node Dysfunction in Heart Failure

Joe Z. Zhang, Nipavan Chiamvimonvat, Guy Perkins, Phung Ngoc Thai, Arianne Caudal, Ryan L. Woltz, Richard Q. Ngo, Hye Sook Shin, Mengjie Xie, Yang Zheng, Daphne A. Diloretto, Yu Liu, Lu Ren, Ebenezer N. Yamoah, Wenshu Zeng, Hao Zhang, Gabriela Grigorean
article en

Abstract

Heart failure (HF) affects approximately 6.2 million people in the United States, with a 5-year mortality exceeding 50%. Bradyarrhythmia, a known complication in HF due to sinoatrial node (SAN) dysfunction (SAND), increases the morbidity and mortality of HF patients. Insights into the mechanistic underpinnings of SAND in HF could therefore uncover vital therapeutic targets to improve clinical outcomes. The SAN cells are endowed with a dense mitochondrial network crucial for sustaining their pacemaking function on a beat-to-beat basis. We have previously demonstrated significant disruptions in the mitochondrial-sarcoplasmic reticulum connectomics, resulting in abnormal mitochondrial Ca <sup>2+</sup> handling and impaired mitochondrial function in HF. Here, we hypothesize that the metabolic perturbation is one of the critical mechanisms underlying SAND. To this end, we took advantage of a multi-omics approach combined with ultra-resolution imaging and functional analyses to decipher the metabolic shift that transpires in the HF SAN. Our findings revealed significant metabolic remodeling within the SAN mitochondria in HF, with a diminished reliance on fatty acid β-oxidation, enhanced utilization of ketone bodies, and heightened dependence on carbohydrate catabolism. Notably, metabolomics analyses identified the pronounced increase of glucosylceramides and ceramides as one of the mechanisms leading to mitochondrial dysfunction. We directly test this hypothesis and demonstrate that ceramides induce a dose-dependent metabolic shift from oxidative phosphorylation to glycolysis. Importantly, these alterations lead to a significant impairment in SAN automaticity in a dose-dependent manner. Collectively, the findings support the notion that ceramides are not only markers of metabolic derangement, but also active mediators of mitochondrial and metabolic dysfunction in the SAN. Overall, the study provides evidence that ceramides may be a potential therapeutic target for mitigating SAND in HF.

bioRxiv (Cold Spring Harbor Laboratory)
University of Arizona (US), University of California, Los Angeles (US), University of Phoenix (US), Cardiovascular Institute of the South (US), University of California San Diego (US), Stanford Medicine (US), Phoenix College (US), University of California, Davis (US), Stanford University (US)
Good health and well-being
Openalex Percentile: Top 63%
Cardiovascular Function and Risk Factors
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