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Leptin, produced by adipose tissue and the placenta, acts as an integrative signal linking maternal energy status with trophoblast function and vascular adaptation, while cholesterol provides essential structural and hormonal substrates required for steroidogenesis and neurodevelopment. Emerging evidence indicates that leptin and cholesterol act as convergent regulators of metabolic and cardiovascular (CV) adaptation during pregnancy. We propose that excessive hyperleptinaemia and maternal hypercholesterolaemia, frequently coexisting, form a convergent axis that modulates placental signalling, alters the epigenetic regulation of lipid transporters and disrupts mitochondrial homeostasis. Mechanistically, this convergence operates through hepatic, epigenetic and renal pathways detailed throughout this review. Beyond the placenta, dysregulation of the leptin\u2013cholesterol axis may extend to maternal organs central to CV homeostasis, particularly the kidney. Emerging evidence suggests that similar leptin\u2010driven renal pathways may operate during pregnancy, amplifying vascular dysfunction and susceptibility to hypertensive complications. This perspective highlights the leptin\u2013cholesterol axis as a mechanistic link connecting placental, kidney and CV pathways within the Developmental Origins of Health and Disease (DOHaD) paradigm, with potential implications for long\u2010term cardiometabolic risk. This review integrates molecular, epigenetic and clinical evidence to emphasize lipoprotein\u2010centred mechanisms, identify critical knowledge gaps and discuss translational opportunities for nutritional intervention, biomarker development and early\u2010life preventive strategies.<\/jats:p>","DOI":"10.1113\/ep093766","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T08:14:06Z","timestamp":1786436046000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Leptin\u2013cholesterol crosstalk in pregnancy: Mechanistic implications for placental function and cardiometabolic programming"],"prefix":"10.1113","author":[{"given":"Julio","family":"Flores","sequence":"first","affiliation":[{"name":"Escuela de Tecnolog\u00eda M\u00e9dica, Facultad de Ciencias Universidad San Sebasti\u00e1n  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diego","family":"Gumera","sequence":"additional","affiliation":[{"name":"Escuela de Tecnolog\u00eda M\u00e9dica, Facultad de Ciencias Universidad San Sebasti\u00e1n  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreina","family":"Arias","sequence":"additional","affiliation":[{"name":"Escuela de Tecnolog\u00eda M\u00e9dica, Facultad de Ciencias Universidad San Sebasti\u00e1n  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristi\u00e1n A.","family":"Amador","sequence":"additional","affiliation":[{"name":"Escuela de Tecnolog\u00eda M\u00e9dica, Facultad de Ciencias Universidad San Sebasti\u00e1n  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda Jos\u00e9","family":"Ya\u00f1ez","sequence":"additional","affiliation":[{"name":"Escuela de Tecnolog\u00eda M\u00e9dica, Facultad de Ciencias Universidad San Sebasti\u00e1n  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,11]]},"reference":[{"key":"e_1_2_13_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02883"},{"key":"e_1_2_13_3_1","first-page":"OL323","article-title":"Leptin, leptin resistance and endothelial dysfunction in pre\u2010eclampsia","volume":"48","author":"Anderson C. 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