& Korst, A
Mechanistic investigations in the field have traditionally focused on single components, such as oocyte mitochondrial dysfunction [11, 12], local microenvironmental alterations [13,14,15], or epigenetic abnormalities [16,17,18]
Nichols E, Steinmetz JD, Vollset S, et al

At the cellular level, GLP-1 agonists exert several beneficial effects: Cardiomyocyte protection : GLP-1 agonists inhibit receptor-interacting protein kinase 3/mixed lineage kinase domain-like pseudokinase-mediated myocardial necroptosis by activating the GLP-1R/PI3K/Akt pathway [5] Anti-fibrotic effects : These agents alleviate cardiac fibrosis and hypertrophy by upregulating atrial natriuretic peptide expression, which suppresses the calcineurin/nuclear factor of activated T cells 3 signaling pathway [5] Cellular stress reduction : GLP-1 agonists diminish endoplasmic reticulum stress and enhance autophagy in cardiomyocytes, preventing apoptosis and blocking progression to heart failure [5] Vascular effects : In vascular smooth muscle cells, GLP-1R activation primarily leads to Gs-mediated cAMP/PKA signaling while simultaneously inhibiting pro-proliferative pathways including ERK1/2 and p38 MAPK [4] Beyond these direct cellular effects, GLP-1 agonists improve cardiac function through multiple systemic mechanisms

24 weeks: Reduction in surface dullness, improved hydration, some fading of very recent postinflammatory hyperpigmentation (PIH) for some individuals