{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPPARδ (PPARD) is a pivotal nuclear receptor in metabolic regulation. It orchestrates lipid metabolism by enhancing fatty acid catabolism and energy uncoupling in tissues such as skeletal muscle, liver, heart, and adipose tissue. Activation of PPARD improves insulin sensitivity and promotes fatty acid oxidation while modulating mitochondrial function and transcriptional programs – for example, via induction of Insig‐1 to repress lipogenesis and regulation of pyruvate dehydrogenase kinase expression during nutrient stress. These actions support its potential as a therapeutic target for obesity, type 2 diabetes, and other features of the metabolic syndrome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its metabolic roles, PPARD exerts significant anti‐inflammatory and homeostatic functions in various cell types. In macrophages, PPARD is induced during the phagocytosis of apoptotic cells, where it acts as a transcriptional sensor to upregulate opsonins and suppress pro‐inflammatory cytokine production, thereby helping to maintain self‐tolerance. In endothelial cells and vascular progenitors, receptor activation blunts chemokine signaling and reduces inflammatory cascades, contributing to diminished atherosclerotic lesion progression. In the skin, PPARD activation stimulates keratinocyte differentiation, enhances barrier homeostasis, and modulates wound repair. Moreover, crosstalk with other nuclear receptors (for example, the vitamin D receptor) and regulation by diverse molecular partners underscore PPARD’s role in fine‐tuning both proliferative and inflammatory responses in a variety of tissues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, context‐dependent PPARD activity is implicated in tumorigenesis. In gastrointestinal models, pharmacological activation of PPARD has been associated with enhanced intestinal adenoma growth and suppression of apoptotic pathways in colorectal cancer cells. In parallel, increased PPARD translation—mediated by epitranscriptomic modifications in hepatocellular carcinoma—drives pro‐oncogenic signaling cascades. Furthermore, PPARD signaling interacts with pathways regulating angiogenic and invasive factors (for example, ANGPTL4), thereby promoting cancer cell invasion in selected contexts. 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