Bioactive factors in endometriosis peritoneal fluid remodel human cardiomyocytes

Jadyn Simon, Elaina Blickenstaff, Mitchell B, Brenda Mitchell, Kristin Sinning, Sinning K, Nalini Santanam
American journal of physiology. Heart and circulatory physiology · 2026 · vol. 331(1) , pp. H89–H97 · doi:10.1152/ajpheart.00259.2026 · PMID:42172437 · PMC13325114 · W7162102296
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

Endometriosis peritoneal fluid, compared to control fluid, increased cardiomyocyte beating frequency, altered sarcomere organization, and shifted gene expression pathways, indicating a cell-intrinsic link to cardiac signaling states.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-08-13 · read from full text ⓘ

This study investigated whether peritoneal fluid from women with endometriosis alters the behavior of human-induced pluripotent stem cell-derived cardiomyocytes in vitro. Exposure to endometriosis-associated peritoneal fluid resulted in increased beating frequency, altered sarcomere organization, and significant changes in gene expression related to adrenoceptor and G protein-coupled receptor signaling pathways compared to control fluids. The authors note that outcomes were condition-dependent rather than uniformly significant, highlighting a complex interaction between the fluid components and cardiac cellular structures. This paper is centrally about endometriosis — specifically examining how its associated peritoneal fluid influences cardiomyocyte function and gene expression as a potential mechanism for increased cardiovascular disease risk in these patients.

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Abstract

Endometriosis is associated with increased cardiovascular disease (CVD) risk, yet the cellular basis for this relationship remains unclear. We examined whether peritoneal fluid (PF) from women with endometriosis alters cardiomyocyte behavior in vitro. Human-induced pluripotent stem cell-derived cardiomyocytes were exposed for 48 h to standard or hypertrophic media supplemented with peritoneal fluid from endometriosis or control patients. Beating frequency was measured using calcium transient imaging, differential gene expression was assessed with the Human CVD-PCR array, and sarcomere features were quantified using gray-level cooccurrence matrix (GLCM)-based texture analysis. Under standard conditions, PF increased beats per minute compared with media alone (control P = 0.0006; endometriosis P < 0.0001), and beating frequency was higher with endometriosis PF than with control PF (P = 0.0214). Sarcomere length increased, and organization metrics reduced following PF (endo and ctrl) exposure under baseline conditions (P 40% of the genes were altered by Endo-PF vs. <10% by control-PF, compared with media-alone treatment. Network analysis showed enrichment of adrenoceptor and G protein-coupled receptor signaling pathways. An increased expression of STAT1 (2.49-fold, P = 0.016) and reduced G0S2 (-5.24-fold, P = 0.037), along with regulation of MYH6 and NPR2, was seen when Endo-PF was compared with Ctrl-PF. In hypertrophic media, PF treatment produced significant differences in sarcomere organization. Outcomes were condition-dependent rather than uniformly significant. Endometriosis-associated PF shifts in cardiomyocyte function, gene expression, and sarcomere structure. This supports a cell-intrinsic link between endometriosis and altered cardiac signaling states and carries implications concerning long-term cardiovascular morbidity and mortality in women with endometriosis.NEW & NOTEWORTHY Endometriosis is linked to cardiovascular disease, but its direct effects on the heart are not well understood, reflecting broader mechanistic gaps in the disease. This study shows that exposure to peritoneal fluid (PF) from women with endometriosis is sufficient to change human cardiomyocyte beating frequency, sarcomere organization, and cardiovascular disease-associated gene expression in vitro. These findings support a cell-intrinsic mechanism through which endometriosis-associated factors may influence cardiac signaling and structure, extending beyond or supporting epidemiologic associations.
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Abstract

Endometriosis is associated with increased cardiovascular disease (CVD) risk, yet the cellular basis for this relationship remains unclear. We examined whether peritoneal fluid (PF) from women with endometriosis alters cardiomyocyte behavior in vitro. Human-induced pluripotent stem cell-derived cardiomyocytes were exposed for 48 hours to standard or hypertrophic media supplemented with peritoneal fluid from endometriosis or control patients. Beating frequency was measured using calcium transient imaging, differential gene expression was assessed with the Human CVD-PCR array, and sarcomere features were quantified using GLCM-based texture analysis. Under standard conditions, PF increased beats per minute compared with media alone (control p=0.0006; endometriosis p < 0.0001), and beating frequency was higher with endometriosis PF than with control PF (p=0.0214). Sarcomere length increased, and organization metrics reduced following PF (endo and ctrl) exposure under baseline conditions (p 40% of the genes were altered by Endo-PF vs. <10% by control-PF, compared to media-alone treatment. Network analysis showed enrichment of adrenoceptor and G protein-coupled receptor signaling pathways. An increased expression of STAT1 (2.49-fold, p=0.016) and reduced G0S2 (-5.24-fold, p=0.037), along with regulation of MYH6 and NPR2, was seen when Endo-PF was compared to Ctrl-PF. In hypertrophic media, PF treatment produced significant differences in sarcomere organization. Outcomes were condition-dependent rather than uniformly significant. Endometriosis-associated PF shifts in cardiomyocyte function, gene expression, and sarcomere structure. This supports a cell-intrinsic link between endometriosis and altered cardiac signaling states and carries implications concerning long-term cardiovascular morbidity and mortality in women with endometriosis. Formats available You can view the full content in the following formats: Information & Authors Information Published In American Journal of Physiology-Heart and Circulatory Physiology Articles in Press Copyright Copyright © 2026 The Authors. Licensed under Creative Commons Attribution CC-BY-NC-ND 4.0. Published by the American Physiological Society. History Received: 30 March 2026 Revised: 10 April 2026 Accepted: 19 May 2026 Published online: 22 May 2026

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Condition tags

endometriosis

MeSH descriptors

Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid Ascitic Fluid

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (39)

SciLite annotations

organisms 5
human noordeloos 2009062 human human human
chemicals 1
calcium

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