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The effect of long-term administration of green tea catechins on aging-related cardiac diastolic dysfunction and decline of troponin I



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Fig 1: Long-term EGCG intake alleviates aging-related cardiomyocyte apoptosis and mitochondrial damage. (A, B) Representative histology of heart tissue sections stained with hematoxylin-eosin stain and Masson's trichrome stain (yellow arrows collagen fibrosis; scale bar: 100 μm). (C) TUNEL stain for evaluation of cardiomyocyte apoptosis (red arrows apoptotic cells; 400 × ). (D) Transmission electron microscope (TEM) for the display of myocardial ultrastructure (blue arrows damaged mitochondria and orange arrows twisted myofilaments; 10000 × ). (E–G) Quantitative analysis of myocardial fibrosis, cardiomyocyte apoptosis, and mitochondrial destruction (n = 3–4). All results are represented as mean ± standard deviation. ∗∗∗P < 0.001.

 

 

 

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Credit: Genes & Diseases




A new publication from Genes & DiseasesDOI  10.1016/j.gendis.2024.101284, discusses the effect of long-term administration of green tea catechins on aging-related cardiac diastolic dysfunction and decline of troponin I.

 

Aging is an independent risk factor for cardiovascular diseases. Cardiac diastolic dysfunction (CDD), ultimately leading to heart failure with preserved ejection fraction (HFpEF), is prevalent among older individuals. Although therapeutics have made great progress, preventive strategies remain unmet medical needs.

 

Green tea catechins have been shown to be effective in improving aging-related cardiovascular and cerebral disorders in animal models and patients. However, little attention has been paid to whether long-term administration of epigallocatechin gallate (EGCG), the major bioactive ingredient of green tea catechins, could prevent the onset and progression of CDD.

 

In this study, 12-month-old female mice were orally administered 50, 100 and 200 mg EGCG mixed with drinking water for 6 months. Aged mice (18 months old) exhibited the major features of HFpEF, including CDD with pEF, cardiac fibrosis, increased cardiomyocyte apoptosis, and mitochondrial damages, as well as elevated A/B-type natriuretic peptide. Cardiac troponin I (cTnI) expression was also reduced. Long-term administration of 100 or 200 mg EGCG prevented aging-related CDD and exercise capacity decline, along with alleviating myocardial apoptosis and mitochondria damage. The transcription and protein expression of cTnI were increased, which might be achieved by inhibiting the expression and activity of histone deacetylase 1 (HDAC1), and reducing its binding level near cTnI's promoter, thereby elevating acetylated histone 3 (AcH3) and acetylated lysine 9 on histone H3 (AcH3K9) in the aged mice.

 

This article reports a novel insight that long-term administration of EGCG is a potentially effective strategy in preventing aging-related CDD and cTnI expression decline.

 

Keywords: Aging, Cardiac diastolic dysfunction, Cardiac troponin I, Epigallocatechin gallate, Histone deacetylase 1

 

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Genes & Diseases publishes rigorously peer-reviewed and high quality original articles and authoritative reviews that focus on the molecular bases of human diseases. Emphasis is placed on hypothesis-driven, mechanistic studies relevant to pathogenesis and/or experimental therapeutics of human diseases. The journal has worldwide authorship, and a broad scope in basic and translational biomedical research of molecular biology, molecular genetics, and cell biology, including but not limited to cell proliferation and apoptosis, signal transduction, stem cell biology, developmental biology, gene regulation and epigenetics, cancer biology, immunity and infection, neuroscience, disease-specific animal models, gene and cell-based therapies, and regenerative medicine.

Scopus CiteScore: 7.3

Impact Factor: 6.9

 

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Print ISSN: 2352-4820

eISSN: 2352-3042

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Junjun Quan, Zhongli Jia, Lingjuan Liu, Jie Tian, The effect of long-term administration of green tea catechins on aging-related cardiac diastolic dysfunction and decline of troponin I, Genes & Diseases, Volume 12, Issue 2, 2025, 101284, ISSN 2352-3042, https://doi.org/10.1016/j.gendis.2024.101284

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