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September 5, 2026MetabolitesOpen Access

Estrogen degradation metabolites induce cardiac hypertrophy and fibrosis by increasing oxidative stress.

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Population

Rat H9c2 cardiomyoblast cells and intact and oophorectomized (Oopho) female rats

Comparison

Exposure to two exogenous estrogenic… vs Control (unexposed cells/rats)

Design

Preclinical

Key result

Exposure to estrogen degradation metabolites, particularly Met D, significantly decreased antioxidant capacity and increased oxidative stress, leading to cardiac hypertrophy and fibrosis.

Authors

ASAlejandro Silva‐PalaciosGNGabriela Navarrete-AnastasioELElizabeth Lira‐Silva

Discussion

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Overview

Met D may promote oxidative stress, hypertrophy, and fibrosis in estrogen-deficient rat hearts despite preserved function; leaves open human relevance and requires prospective study.

Key Points

  • To evaluate the in vitro cellular effects and in vivo cardiac impact of two estrogen degradation metabolites, 2-hydroxyestrone (Met A) and 17β-estradiol-3-methyl-ether (Met D), in cardiac cells and oophorectomized female rats.
  • Exposed rat H9c2 cardiomyoblast cells to varying concentrations and durations of Met A and Met D to evaluate cell viability, mitochondrial membrane potential, and oxidative stress.
  • Administered Met A and Met D to intact and oophorectomized (Oopho) female rats to assess heart function via echocardiography, histological tissue remodeling, and markers of cardiac oxidative damage.
  • Met D induced the most pronounced adverse cellular effects in vitro, significantly reducing antioxidant capacity while elevating oxidative stress.
  • Echocardiographic assessments showed unchanged global cardiac pump function across animal groups, but histological analyses revealed clear signs of cardiac hypertrophy and fibrosis.

Structured PICO

P
Population
Female rats (intact and oophorectomized) and rat H9c2 cardiomyoblast cells exposed to estrogen degradation metabolites.
I
Intervention
Exposure to two exogenous estrogenic metabolites (EDMs): Met A (2-hydroxyestrone) and Met D (17β-estradiol-3-methyl-ether)
C
Comparator
Control (unexposed cells/rats)
O
Outcome
Cell viability, mitochondrial potential, and oxidative stress in H9c2 cells; echocardiographic analyses, histological analyses, cardiac damage, and oxidative stress in intact and Oopho ratssurrogate

Exogenous estrogenic metabolites, particularly 17β-estradiol-3-methyl-ether, induce oxidative stress, cardiac hypertrophy, and fibrosis in female rat models without altering echocardiographic cardiac function.

Cite This Study

Silva‐Palacios et al. (2026) studied this question. Estrogen degradation metabolites (Met A and Met D) was evaluated on Cell viability, mitochondrial potential, oxidative stress, and cardiac function/histology. Exposure to estrogen degradation metabolites, particularly Met D, significantly decreased antioxidant capacity and increased oxidative stress, leading to cardiac hypertrophy and fibrosis.

synapsesocial.com/papers/6a9bd48c6b95aff0620ec3f2https://doi.org/10.3390/metabo16090647
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract Thu156: Impacts of Estradiol and Progesterone On Cardiomyocyte Cell Dynamics and Mitochondrial Respiration2025
  2. 2Abstract Thu153: Divergent Sex-Specific Effects of Estrogen on Cardiac Function: The Intersection of Adora2b Signaling and IL-6 Regulated Ferroptosis2025
  3. 3Antioxidant, Bioenergetic, and Metabolic Effects of Novel Mitochondria-Targeted Estrogens2025
  4. 4Abstract Thu164: Sexual Dimorphism In the Cardiac Response To Methamphetamines2025
  5. 5A Supra-Physiological Dose of 2-Hydroxyestradiol Impairs Meiotic Progression and Developmental Competence of Mouse Antral Oocytes2025