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Upon ligand recognition, <jats:styled-content style=\"fixed-case\">NOD1<\/jats:styled-content> undergoes conformational changes and self\u2010oligomerization mediated by the nucleotide\u2010binding <jats:styled-content style=\"fixed-case\">NACHT<\/jats:styled-content> domains, followed by the recruitment and activation of the serine threonine kinase receptor\u2010interacting protein 2 leading to the activation of <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> pathways and induction of inflammatory genes. Much of our knowledge is derived from seminal studies using mice deficient in <jats:styled-content style=\"fixed-case\">NOD1<\/jats:styled-content> and confirming an essential role for <jats:styled-content style=\"fixed-case\">NOD1<\/jats:styled-content> in the host immune response against gastrointestinal and respiratory pathogens. In addition, recent studies have revealed a role for intracellular <jats:styled-content style=\"fixed-case\">NOD1<\/jats:styled-content> receptors in the regulation of vascular inflammation and metabolism. This review will discuss our current understanding of intracellular <jats:styled-content style=\"fixed-case\">NOD1<\/jats:styled-content> receptors in host immunity and chronic inflammatory disorders with a focus on cardiovascular diseases. 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