White Adipose Tissue in Obesity-Associated HFpEF

Obesity and hypertension are prevalent comorbidities in heart failure with preserved ejection fraction (HFpEF). Increased adiposity is implicated in its pathophysiology. We investigated changes in white adipose tissue (WAT) in obesity-associated HFpEF utilizing patient samples and a murine model of obesity-associated HFpEF. WAT analysis revealed "browning", characterized by smaller adipocytes and increased UCP1 expression, alongside fibrosis and reduced vascular markers during acute HF decompensation. During chronic, stable HFpEF, "browning" markers declined. There is a dynamic process in WAT, where acute HF exacerbations trigger transient "browning", fibrosis, and vascular deterioration, which partially reverse but fibrosis persists. WAT dysfunction worsens during acute HF, highlighting a potential therapeutic target for obesity-related HFpEF.

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Publication Details

Journal
JACC Basic to Translational Science
Published
2025-05-08
DOI
https://doi.org/10.1016/j.jacbts.2025.02.021
Citations
2
Primary Topic
Cardiovascular Disease and Adiposity
Type
article
Field-Weighted Citation Impact
2.78

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article

White Adipose Tissue in Obesity-Associated HFpEF

David R. Pimentel, Eng Leng Saw, Flora Sam, María Valero‐Muñoz et al.
2 citations
JACC Basic to Translational Science
Cardiovascular Disease and Adiposity
2.78
article

White Adipose Tissue in Obesity-Associated HFpEF

David R. Pimentel, Eng Leng Saw, Flora Sam, María Valero‐Muñoz, Hannah Cooper
article en
2 citations

Abstract

Obesity and hypertension are prevalent comorbidities in heart failure with preserved ejection fraction (HFpEF). Increased adiposity is implicated in its pathophysiology. We investigated changes in white adipose tissue (WAT) in obesity-associated HFpEF utilizing patient samples and a murine model of obesity-associated HFpEF. WAT analysis revealed "browning", characterized by smaller adipocytes and increased UCP1 expression, alongside fibrosis and reduced vascular markers during acute HF decompensation. During chronic, stable HFpEF, "browning" markers declined. There is a dynamic process in WAT, where acute HF exacerbations trigger transient "browning", fibrosis, and vascular deterioration, which partially reverse but fibrosis persists. WAT dysfunction worsens during acute HF, highlighting a potential therapeutic target for obesity-related HFpEF.

JACC Basic to Translational ScienceVol. 10(8)
Boston University (US)
National Institutes of Health
Zero hunger
Openalex Percentile: Top 10%
Cardiovascular Disease and Adiposity
2.78
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White Adipose Tissue in Obesity-Associated HFpEF — David R. Pimentel, Eng Leng Saw, et al. · JACC Basic to Translational Science (2025) | TGRS Research Map | TGRS