AGT (angiotensinogen)
The AGT gene encodes angiotensinogen, a critical precursor protein that serves as the foundational substrate of the renin-angiotensin system (RAS), a key regulatory network for cardiovascular and renal homeostasis. Primarily synthesized and secreted by hepatocytes into the circulation, angiotensinogen undergoes sequential proteolytic processing, first being cleaved by renin to generate angiotensin I, which is subsequently converted into the potent vasoconstrictor angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II exerts its physiological effects by binding to specific G-protein-coupled receptors, notably AT1 and AT2, thereby modulating systemic blood pressure, fluid volume, and electrolyte balance through mechanisms such as vasoconstriction, aldosterone secretion, and sympathetic nervous system activation. Beyond its classical role in hemodynamic regulation, the RAS, and by extension AGT, is implicated in broader cellular processes including inflammation, cell proliferation, and tissue fibrosis. Although AGT is phylogenetically classified within the serine protease inhibitor (serpin) superfamily due to shared structural motifs, it diverges functionally from typical serpins by acting primarily as a hormone precursor rather than a direct enzyme inhibitor. Genetic variations in AGT, such as specific single nucleotide polymorphisms, can alter expression levels or protein function, thereby influencing susceptibility to pathological conditions including primary hypertension, preeclampsia, and chronic kidney disease. Dysregulation of AGT expression has significant clinical implications; overexpression leads to elevated angiotensin II levels, exacerbating vascular resistance and contributing to cardiovascular and renal damage, whereas reduced expression may lower blood pressure but risks disrupting essential fluid and electrolyte homeostasis if excessively suppressed.
Gene Ontology
Subcellular localization of AGT (and its protein):
- plasma membrane
- cytoplasm
- extracellular
- golgi
- vesicle
- cytoskeleton
- endoplasmic reticulum
- nucleus
- endosome
- lysosome
- mitochondrion
Gene Ontology (GO) terms for AGT:
| Interacting Gene | Interaction | Source/Score |
| Name |
|---|
| 4614 Renin-angiotensin system [PATH:hsa04614] |
| 4270 Vascular smooth muscle contraction [PATH:hsa04270] |
| 5410 Hypertrophic cardiomyopathy (HCM) [PATH:hsa05410] |
| Name |
|---|
| Class A/1 (Rhodopsin-like receptors) |
| Fatty acid, triacylglycerol, and ketone body metabolism |
| G alpha (i) signalling events |
| G alpha (q) signalling events |
| Gastrin-CREB signalling pathway via PKC and MAPK |
| GPCR downstream signaling |
| GPCR ligand binding |
| Metabolism |
| Metabolism of Angiotensinogen to Angiotensins |
| Metabolism of lipids and lipoproteins |
| Metabolism of proteins |
| Peptide hormone metabolism |
| Peptide ligand-binding receptors |
| PPARA activates gene expression |
| Regulation of lipid metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha) |
| Signal Transduction |
| Signaling by GPCR |
| Disease | Score | NofPmids | NofSnps | Source |
| Allanson Pantzar McLeod syndrome | 0.480271442 | 3 | 3 | BeFree_CLINVAR_CTD_human_ORPHANET_UNIPROT |
| Hypertensive disease | 0.44 | 546 | 5 | BeFree_CTD_human_GAD_LHGDN_RGD |
| Myocardial Infarction | 0.247263357 | 53 | 0 | BeFree_CTD_human_GAD_LHGDN_RGD |
| Atherosclerosis | 0.240705144 | 57 | 1 | BeFree_CTD_human_GAD_LHGDN_RGD |
| Liver Cirrhosis | 0.217826744 | 7 | 1 | BeFree_CTD_human_GAD_LHGDN_RGD |
| Heart failure | 0.216525617 | 32 | 0 | BeFree_CTD_human_GAD_RGD |
| Diabetic Retinopathy | 0.20827274 | 8 | 0 | BeFree_CTD_human_GAD_LHGDN_RGD |
| Fibrosis | 0.207458414 | 7 | 0 | CTD_human_GAD_LHGDN_RGD |
| Focal glomerulosclerosis | 0.203538676 | 5 | 0 | BeFree_CTD_human_LHGDN_RGD |
| Cardiomegaly | 0.2 | 16 | 0 | CTD_human_RGD |
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