ArticleNature cardiovascular research2024
Semaphorin-3A regulates liver sinusoidal endothelial cell porosity and promotes hepatic steatosis.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- Endothelial cell LGR4 maintains liver sinusoidal endothelial cell Identity and protects against hepatic steatosis.Life sciences · 2026Article
- The liver in diabetes: current state and future perspectives.Diabetologia · 2026Review
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- High-fat diet feeding induces organ-specific vascular remodeling with distinct temporal dynamics in male mice.Communications biology · 2026Article
- Lipid remodeling and circulating semaphorin 3A in diminished ovarian reserve.Scientific reports · 2026Article
- Serum Semaphorin Alterations in Psoriasis: Links to Metabolic Status Rather than Disease Severity.Metabolites · 2026Article
- Pulsed electromagnetic fields mediate sensory nerve regulation for bone formation in aging models.Nature communications · 2025Article
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- Loss of endothelial ZEB2 in mice attenuates steatosis early during metabolic dysfunction-associated steatotic liver disease.Scientific reports · 2025Article
- Obesity drives depot-specific vascular remodeling in male white adipose tissue.Nature communications · 2025Article
- Blood flow-induced angiocrine signals promote organ growth and regeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, increases worldwide and associates with type 2 diabetes and other cardiometabolic diseases. Here we demonstrate that Sema3a is elevated in liver sinusoidal endothelial cells of animal models for obesity, type 2 diabetes and MASLD. In primary human liver sinusoidal endothelial cells, saturated fatty acids induce expression of SEMA3A, and loss of a single allele is sufficient to reduce hepatic fat content in diet-induced obese mice. We show that semaphorin-3A regulates the number of fenestrae through a signaling cascade that involves neuropilin-1 and phosphorylation of cofilin-1 by LIM domain kinase 1. Finally, inducible vascular deletion of Sema3a in adult diet-induced obese mice reduces hepatic fat content and elevates very low-density lipoprotein secretion. Thus, we identified a molecular pathway linking hyperlipidemia to microvascular defenestration and early development of MASLD.
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Registered trials
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