| Biomarker | Renin | Full name | Renin | Molecular Type | Protein (protease) |
| Molecular Formula | / | Molecular Weight | 37 kDa | Core Functional Dimensions | Diagnosis, susceptibility, monitoring |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum/plasma (radioimmunoassay, ELISA, chemiluminescence) | ||
| Pathobiological Mechanisms | Catalytic angiotensin into its angiotensin I, start the RAAS pathways, regulating the blood pressure steady | ||||
| Clinical Availability Status | Clinical availability (primary/secondary hypertension differentiation) | ||||
| Notes and Dynamics | Joint detection and aldosterone ratio (ARR) is the core of primary aldosteronism screening index, the secretion is regulated by the sodium intake and blood pressure changes | ||||
| Biomarker | Aldosterone | Full name | Aldosterone | Molecular Type | Steroid hormones (protein derivatives) |
| Molecular Formula | / | Molecular Weight | 360.45 Da | Core Functional Dimensions | Diagnosis, susceptibility, prognosis, monitoring |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Adrenal cortex | Test Sample / Technology Platform | Serum/plasma (ELISA, mass spectrometry, radioimmunoassay) | ||
| Pathobiological Mechanisms | Activated RAAS system, promote the renal sodium water retention, vascular smooth muscle contraction, induced myocardial and vascular fibrosis | ||||
| Clinical Availability Status | Clinically available (secondary hypertension diagnosis, treatment monitoring) | ||||
| Notes and Dynamics | It is a key driver of refractory hypertension. Aldosterone receptor antagonist (spironolactone, eplerenone) is the first-line treatment drug and is closely related to obesity-related hypertension | ||||
| Biomarker | ICAM-1 | Full name | Intercellular adhesion molecule 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 80-110 kDa | Core Functional Dimensions | Susceptibility, monitoring |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, epithelial cells | Test Sample / Technology Platform | Serum/plasma (ELISA, immunoturbidimetry) | ||
| Pathobiological Mechanisms | It can enhance the adhesion and migration of white blood cells to endothelial cells, activate inflammatory signaling pathways, and aggravate vascular injury | ||||
| Clinical Availability Status | Clinical exploration/research validation: used to evaluate the inflammatory state of blood vessels in hypertension, some used in clinical research | ||||
| Notes and Dynamics | ICAM-1 neutralizing antibody can reduce the blood pressure of hypertension model, provide new ideas for targeted therapy | ||||
| Biomarker | VCAM 1 | Full name | Vascular cell adhesion molecule 1 | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | 100-110 kDa | Core Functional Dimensions | Susceptibility, monitoring |
| Disease(or Constitution) | PCOS | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells | Test Sample / Technology Platform | Serum/plasma (ELISA and western blot method) | ||
| Pathobiological Mechanisms | Mediated immune cells and vascular endothelial adhesion, inflammation cells infiltration, increase vascular inflammation and reconstruction | ||||
| Clinical Availability Status | The validation: associated with progression of hypertension and target organs damage, clinical application is limited | ||||
| Notes and Dynamics | And blood pressure variability is related to the level of its can be used as early markers of endothelial dysfunction | ||||
| Biomarker | VCAM 1 | Full name | Vascular cell adhesion molecule 1 | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | 100-110 kDa | Core Functional Dimensions | Susceptibility, monitoring |
| Disease(or Constitution) | PCOS | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells | Test Sample / Technology Platform | Serum/plasma (ELISA and western blot method) | ||
| Pathobiological Mechanisms | Mediated immune cells and vascular endothelial adhesion, inflammation cells infiltration, increase vascular inflammation and reconstruction | ||||
| Clinical Availability Status | The validation: associated with progression of hypertension and target organs damage, clinical application is limited | ||||
| Notes and Dynamics | And blood pressure variability is related to the level of its can be used as early markers of endothelial dysfunction | ||||
| Biomarker | CCL2/MCP-1 | Full name | Monocyte chemoattractant protein-1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 13 kDa | Core Functional Dimensions | Susceptibility, monitoring |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, macrophages, smooth muscle cells | Test Sample / Technology Platform | Serum/plasma (ELISA, multiplex immunoassays) | ||
| Pathobiological Mechanisms | Chemokines monocyte infiltration blood vessels, promote macrophage activation and foam cell formation, accelerate the blood vessel damage | ||||
| Clinical Availability Status | Validation: in high blood pressure is widely used in the research of vascular inflammation and progress is expected to be used to monitor the blood vessel damage | ||||
| Notes and Dynamics | CCR2 antagonists can reduce hypertension model of vascular inflammation, related drugs in preclinical research and development stage | ||||
| Biomarker | TNF alpha | Full name | Tumor necrosis factor alpha | Molecular Type | Proteins |
| Molecular Formula | / | Molecular Weight | 17 kDa | Core Functional Dimensions | Susceptibility, prognosis |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Macrophages, monocytes, T cells | Test Sample / Technology Platform | Serum/plasma (ELISA, chemiluminescence) | ||
| Pathobiological Mechanisms | It activates inflammatory pathways in vascular endothelial cells, increases vascular permeability, induces oxidative stress and vasoconstriction | ||||
| Clinical Availability Status | Research validation/clinical exploration: It is used to evaluate the degree of inflammation in hypertension, but has not been routinely used in clinical practice | ||||
| Notes and Dynamics | Related to vascular stiffness in patients with hypertension, biological agents targeting TNF-α have shown antihypertensive potential in experimental models | ||||
| Biomarker | IL-6 | Full name | Interleukin-6 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 21 kDa | Core Functional Dimensions | Susceptibility, prognosis, surveillance |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Immune cells , hepatocytes | Test Sample / Technology Platform | Serum/plasma (ELISA, flow cytometry) | ||
| Pathobiological Mechanisms | It mediates inflammatory cascades, induces vascular smooth muscle cell proliferation, endothelial dysfunction, and promotes vascular remodeling | ||||
| Clinical Availability Status | Research validation/clinical application: It is widely used in the study of inflammatory mechanisms of hypertension, and partly used in the stratification of high-risk patients | ||||
| Notes and Dynamics | It is a key inflammatory mediator in hypertension complicated with metabolic syndrome. Anti-il-6 therapy may provide a new direction for refractory hypertension | ||||
| Biomarker | hs-CRP | Full name | High-sensitivity C-reactive protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 11.6 kDa | Core Functional Dimensions | Susceptibility, prognosis, surveillance |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Liver | Test Sample / Technology Platform | Serum/plasma (immune turbidimetry, ELISA) | ||
| Pathobiological Mechanisms | Inflammatory reaction activation, and promote the vascular endothelial injury and vascular remodeling and oxidative stress, increased blood pressure | ||||
| Clinical Availability Status | Clinically available (risk assessment, prognosis) | ||||
| Notes and Dynamics | It is closely related to hypertension target organ damage (heart, kidney, blood vessels), and is expected to be used as a monitoring index for anti-inflammatory treatment | ||||
| Biomarker | NSE | Full name | Neuron-specific enolase | Molecular Type | Protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNENs (Universal) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Immunoassay) | ||
| Pathobiological Mechanisms | Neuroendocrine cell-specific enolase, reflecting tumor burden and differentiation degree | ||||
| Clinical Availability Status | Clinical assistance: 30-50% PanNENs were elevated, and those with G3 and metastasis had higher levels. Combined with CgA, the disease progression was monitored | ||||
| Notes and Dynamics | The specificity of CgA is lower than that of CgA, and interferons such as neurogenic tumors should be excluded | ||||
| Biomarker | Ki-67 | Full name | Ki-67 antigen | Molecular Type | Protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Grading, prognosis |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNENs (Universal) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue (IHC, digital pathology analysis) | ||
| Pathobiological Mechanisms | Cell proliferation markers, reflecting tumor proliferation activity | ||||
| Clinical Availability Status | The guidelines mandatory requirements: WHO grading core indicators (G1: <3%, G2:3-20%, G3: >20%); Numerical analysis can reduce observer variability | ||||
| Notes and Dynamics | It is the core basis for the selection of treatment options, and it can optimize the prognosis prediction combined with clinical staging | ||||
| Biomarker | RB1 | Full name | Retinoblastoma gene 1 | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis and prognosis |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNEC (poorly differentiated, G3) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue (IHC, NGS) | ||
| Pathobiological Mechanisms | Retinoblastoma gene, deletion results in uncontrolled cell cycle and accelerates tumor progression | ||||
| Clinical Availability Status | In clinical validation, PanNEC characteristic deletion combined with TP53 mutation to predict chemotherapy sensitivity; It was used to exclude PanNET G3 | ||||
| Notes and Dynamics | It is a key differential marker for PanNEC and PanNET G3 | ||||
| Biomarker | TP53 | Full name | TP53 gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis and Prognosis |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNEC (poorly differentiated, G3) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue (IHC, NGS) | ||
| Pathobiological Mechanisms | Tumor suppressor genes, mutations lead to uncontrolled cell cycle checkpoints and enhance invasiveness | ||||
| Clinical Availability Status | Clinical differential core: 90% PanNEC mutation, used to distinguish between PanNET G3 and PanNEC; The prognosis of Pannec with mutation is extremely poor | ||||
| Notes and Dynamics | Combination with RB1 deletion is a molecular feature of PanNEC, which can guide the choice of platinum-based chemotherapy | ||||
| Biomarker | GAS | Full name | Gastrin | Molecular Type | Hormones |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Monitoring |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNET (functional) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (immunoassay) | ||
| Pathobiological Mechanisms | G cell-derived tumor secretion, causing Zolie-Ellison syndrome (high gastric acid, peptic ulcer) | ||||
| Clinical Availability Status | High clinical specificity: serum level ≥300pg/mL suggests gastrinoma, and patients with MEN1 syndrome should be preferentially screened | ||||
| Notes and Dynamics | The diagnostic sensitivity can be improved when combined with CgA | ||||
| Biomarker | INS | Full name | Insulin | Molecular Type | hormone |
| Molecular Formula | C₂₅₇H₃₈₃N₆₅O₇₇S₆ | Molecular Weight | 5807.6 | Core Functional Dimensions | Diagnosis, Monitoring |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNET (Functional) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (immunoassay) | ||
| Pathobiological Mechanisms | Excessive secretion of β-cell-derived tumors leads to hypoglycemia syndrome | ||||
| Clinical Availability Status | The diagnostic sensitivity was 52-94% in combination with Whipple's triad (hypoglycemia, blood glucose ≤40mg/dL, remission with sugar supplementation) | ||||
| Notes and Dynamics | It is a core diagnostic marker for insulinoma, and monitoring its level after operation can evaluate the efficacy of surgery | ||||
| Biomarker | SSTR2A | Full name | Somatostatin receptor subtype 2A | Molecular Type | Protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Treatment prediction, diagnosis |
| Disease(or Constitution) | Pancreatic Neuroendocrine Tumors | Disease Subtypes | PanNET (well differentiated, G1/G2/G3) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue/serum (IHC, PET/CT) | ||
| Pathobiological Mechanisms | Somatostatin receptor subtypes, which mediate growth inhibitory signals, are highly expressed in PANnets | ||||
| Clinical Availability Status | The guidelines recommend: IHC testing to guide peptide receptor radionuclide therapy (PRRT); 68Ga-DOTATATE PET/CT is used for staging, and patients with high uptake have better efficacy of PRRT | ||||
| Notes and Dynamics | The expression level of PRRT was negatively correlated with Ki-67, and the expression rate of G1/G2 was higher than that of G3 | ||||