ECM Remodeling in Direct Inguinal Hernia: The Role of Aging, Oxidative Stress, and Antioxidants Defenses
Abstract
Inguinal hernia represents a multifactorial condition driven by extracellular matrix (ECM) dysregulation, collagen imbalance, and oxidative stress. Across studies, a consistent reduction in the collagen I:III ratio, coupled with altered expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), underpins weakened fascia and hernia susceptibility. Aging further impairs ECM remodeling through fibroblast senescence, cross-linking deficits, and elastic fiber attrition, while oxidative stress and inflammation amplify tissue degradation and impair repair mechanisms. Evidence from clinical and experimental studies underscores the interplay between surgical technique, mesh choice, redox balance, and recurrence risk. Understanding the combined impact of aging and oxidative stress provides a mechanistic framework for targeted therapeutic and surgical strategies aimed at preventing hernia development and recurrence.
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