| Title: |
From Disease to Pregnancy: Rethinking Cardiac Remodeling Through Fibroblast, Immune Cell, and Hormonal Interactions. |
| Authors: |
Ruggiero, Emily B.; Carver, Wayne; Fan, Daping; Goldsmith, Edie C.; LaVoie, Holly A. |
| Source: |
Cells (2073-4409); May2026, Vol. 15 Issue 9, p778, 29p |
| Subject Terms: |
PREGNANCY; FIBROBLASTS; CELLULAR immunity; VENTRICULAR remodeling; ENDOCRINE system; HEART failure; HEART fibrosis; EXTRACELLULAR matrix |
| Abstract: |
Highlights: What are the main findings? The review emphasizes that pregnancy-associated cardiac remodeling is driven largely by hormonal signals—particularly estrogen, progesterone, prolactin, and relaxin—which promote an adaptive, reversible, and protective remodeling state, characterized by cardiomyocyte hypertrophy, enhanced angiogenesis, modulation of immune cell activation, and controlled extracellular matrix remodeling without net fibrosis. What are the implications of the main findings? Focusing on non-myocyte cell populations and matrix dynamics, this review promotes pregnancy as a physiological system through which endogenous anti-fibrotic processes can be leveraged for therapeutic discovery. Cardiac fibrosis is a central determinant of heart failure progression and arises from pathological remodeling characterized by fibroblast activation, myofibroblast differentiation, and excessive extracellular matrix deposition. In contrast, physiological remodeling permits adaptive cardiac growth without net fibrosis. Pregnancy represents an underexplored physiological model of reversible cardiac remodeling. In response to hemodynamic load, the maternal heart undergoes hypertrophic growth that resolves postpartum, constituting a natural paradigm of fibrosis-resistant cardiac adaptation. Pregnancy and lactation are accompanied by profound endocrine and immune reprogramming of maternal tissues. We propose that this hormonal milieu orchestrates coordinated crosstalk among endothelial cells, fibroblasts, and immune cell populations to suppress profibrotic pathways and preserve extracellular matrix homeostasis. Candidate regulators include estrogen, progesterone, prolactin family peptides, relaxin, oxytocin, and components of the renin–angiotensin–aldosterone system. During the postpartum and lactational period, prolactin and oxytocin may further promote reverse remodeling. These hormones likely act by modulating local cytokine and growth factor networks that otherwise drive fibroblast activation. By focusing on non-myocyte cardiac cells and extracellular matrix dynamics, this review positions pregnancy as a translational model to uncover endogenous anti-fibrotic mechanisms and identify novel therapeutic strategies for cardiac fibrosis. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |