3,3-Dimethyl-1-butanol attenuates cardiac remodeling in pressure-overload-induced heart failure mice

Wang, Guangji; Kong, Bin; Shuai, Wei; Fu, Hui; Jiang, Xiaobo; Huang, He

doi:10.1016/j.jnutbio.2020.108341

Cited by 100Cardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsHeart Failure Treatment and Management

3,3-Dimethyl-1-butanol attenuates cardiac remodeling in pressure-overload-induced heart failure mice

Wang, Guangji, Kong, Bin, Shuai, Wei, Fu, Hui, Jiang, Xiaobo, Huang, He·2020·The Journal of Nutritional Biochemistry

DOI 10.1016/j.jnutbio.2020.108341

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Abstract

Trimethylamine N-oxide (TMAO) is closely related to cardiovascular diseases, particularly heart failure (HF). Recent studies shows that 3,3-dimethyl-1-butanol (DMB) can reduce plasma TMAO levels. However, the role of DMB in overload-induced HF is not well understood. In this research study, we explored the effects and the underlying mechanisms of DMB in overload-induced HF. Aortic banding (AB) surgery was performed in C57BL6/J mice to induce HF, and a subset group of mice underwent a sham operation. After surgery, the mice were fed with a normal diet and given water supplemented with or without 1% DMB for 6 weeks. Cardiac function, plasma TMAO level, cardiac hypertrophy and fibrosis, expression of inflammatory, electrophysiological studies and signaling pathway were analyzed at the sixth week after AB surgery. DMB reduced TMAO levels in overload-induced HF mice. Adverse cardiac structural remodeling, such as cardiac hypertrophy, fibrosis and inflammation, was elevated in overload-induced HF mice. Susceptibility to ventricular arrhythmia also significantly increased in overload-induced HF mice. However, these changes were prevented by DMB treatment. DMB attenuated all of these changes by reducing plasma TMAO levels, hence negatively inhibiting the p65 NF-κB signaling pathway and TGF-β1/Smad3 signaling pathway. DMB plays an important role in attenuating the development of cardiac structural remodeling and electrical remodeling in overload-induced HF mice. This may be attributed to the p65 NF-κB signaling pathway and TGF-β1/Smad3 signaling pathway inhibition.

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Trimethylamine N-oxide has been shown to promote platelet reactivity and thrombosis potential, vascular inflammation and inflammasome activation, and heightened heart failure and chronic kidney disease related phenotypes in animal models.
“It has also been shown to promote platelet reactivity and thrombosis potential14, 83–85, vascular inflammation and inflammasome activation86–88, heightened heart failure89–91 and CKD92–95 related phenotypes in animal models (Figure 2).”
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Abstract 19293: Removal of Dietary Trimethylamine N-Oxide (TMAO) Attenuates Cardiac Dysfunction in Pressure Overload Induced Heart Failure
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Reductions in gut microbiota‑derived metabolite trimethylamine N‑oxide in the circulation may ameliorate myocardial infarction‑induced heart failure in rats, possibly by inhibiting interleukin‑8 secretion
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Nonlethal Inhibition of Gut Microbial Trimethylamine N‐oxide Production Improves Cardiac Function and Remodeling in a Murine Model of Heart Failure
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Abstract 334: Gut Microbiome Derived Trimethyl-n-oxide Exacerbates Inflammation And Induces Cardiac Fibrosis In Human Cardiac Fibroblasts And In Rodent Model Of Cardiorenal Disease
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Abstract 364: Pathological Effects of Trimethylamine N-oxide (TMAO) on Pressure Overload-induced Heart Failure
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Authors: Wang, G., Kong, B., Shuai, W., Fu, H., Jiang, X., & Huang, H.
Affiliations: Wuhan University (CN)
Corresponding author: Huang, He
ORCID: Wang, Guangji
Kong, Bin
Shuai, Wei
Fu, Hui
Jiang, Xiaobo
Huang, He
Venue: The Journal of Nutritional Biochemistry
Publisher: Elsevier BV
Published: 2020-04
Volume: 78
Pages: 108341
ISSN: 0955-2863 (ISSN-L)
DOI: 10.1016/j.jnutbio.2020.108341
OpenAlex: W3000070485
Cited by: 100
References: 37
Citations by year: 2026: 20 · 2025: 28 · 2024: 13 · 2023: 14 · 2022: 9 · 2021: 13 · 2020: 3
FWCI: 6.10
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: The Journal of Nutritional Biochemistry (publishedVersion)
PubMed (publishedVersion)
Funders: National Key Research and Development Program of China (2017YFC1700500)
National Natural Science Foundation of China (81570306, 81570459)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
Keywords: 3,3-dimethyl-1-butanol, trimethylamine N-oxide, heart failure, pressure overload, cardiac remodeling, cardiac hypertrophy, myocardial fibrosis, ventricular arrhythmias, NF-κB signaling, TGF-β1/Smad3 signaling, aortic banding, inflammation, electrophysiological remodeling
MeSH terms: Hexanols, Animals, Disease Models, Animal, Echocardiography, Electrocardiography, Fibroblasts, Heart, Cardiomegaly, Heart Failure, Hemodynamics, Inflammation, Male, Methylamines, Mice, Inbred C57BL, Myocardium, Pressure, Signal Transduction, Ventricular Remodeling, Mice, Transcription Factor RelA, Transforming Growth Factor beta1

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3,3-Dimethyl-1-butanol attenuates cardiac remodeling in pressure-overload-induced heart failure mice

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