| Biomarker | NPM1 mutation | Full name | Nucleophosmin 1 gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, MRD monitoring | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (genomic sequencing, RT-qPCR) | ||
| Pathobiological Mechanisms | The nuclear-cytoplasmic shuttling molecular chaperone protein, when mutated, leads to cytoplasmic mislocalization and abnormal regulation of functions such as ribosome assembly and DNA repair. | ||||
| Clinical Availability Status | Clinical validation/guideline recommendations: Prognostic stratification included in ELN and NCCN guidelines; Core indicators for MRD monitoring. | ||||
| Notes and Dynamics | Single mutations indicate a favorable prognosis, while the presence of FLT3-ITDhigh or IDH1/2 mutations is associated with a poorer prognosis; ATRA+ATO can degrade the mutated protein. | ||||
| Biomarker | miR-1 / miR-133a | Full name | MicroRNA-1 / MicroRNA-133a-1 | Molecular Type | Noncoding RNA (miRNA) |
| Molecular Formula | / | Molecular Weight | 22 nt | Core Functional Dimensions | Diagnosis, prognosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, skeletal muscle | Test Sample / Technology Platform | Serum/plasma (RT-PCR, real-time PCR, digital PCR) | ||
| Pathobiological Mechanisms | Regulation of cardiomyocyte apoptosis, hypertrophy related genes (such as Bcl-2, IGF-1); The expression of myocardial cells is significantly abnormal after myocardial injury | ||||
| Clinical Availability Status | Clinical validation (auxiliary diagnosis) : multicenter studies confirmed the marked increase in AMI onset within 2 h (a fold change 2.65-10), and cTn were positively correlated (r = 0.7), part of the center for cTn negative patients with early auxiliary diagnosis | ||||
| Notes and Dynamics | MiR-133-a diagnosis of AUC 0.928, is superior to the part of the hs-cTn detection; It has good stability (can be stored for 72 hours in serum) and is suitable for sample transport in remote areas | ||||
| Biomarker | GPBB | Full name | Glycogen phosphorylase BB isoenzyme | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | 97 kDa | Core Functional Dimensions | Early Diagnosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, brain | Test Sample / Technology Platform | Serum (ELISA, immune chromatography, chemiluminescence) | ||
| Pathobiological Mechanisms | Myocardial ischemia, activation glycogen decomposition energy, released into the bloodstream after cellular damage; Is a key enzyme glycogen metabolism, the myocardial specificity is higher | ||||
| Clinical Availability Status | Research validation: single-center studies confirmed that the onset of 1-4 h sensitivity is better than that of myoglobin, but not into the mainstream clinical guidelines, only in the center of the part of the cardiovascular specialist for difficult cases | ||||
| Notes and Dynamics | Ischemia, which release (before the cTn), 6-10 h up to the peak, 24 h recovery; And is associated with the degree of myocardial ischemia, can be used to evaluate the myocardial suppression "potential injury patients | ||||
| Biomarker | Myoglobin (Mb) | Full name | Myoglobin (Mb) | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | 17 kDa | Core Functional Dimensions | Early diagnosis and rule out the diagnosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, skeletal muscle | Test Sample / Technology Platform | Serum/plasma (ELISA, POCT, immune chromatography) | ||
| Pathobiological Mechanisms | 1 h is elevated, 4-12 h of peak, 24-48 h restoring baseline; Joint cTn or CK-MB make up for a lack of specificity, high patients avoid misdiagnosis of skeletal muscle injury | ||||
| Clinical Availability Status | Early clinical available (exclude diagnosis) : guidelines recommended for AMI exclude diagnosis within 6 h of stroke onset, negative predictive value (NPV) of more than 90%, emergency POCT platform is widely used | ||||
| Notes and Dynamics | 1 h is elevated, 4-12 h of peak, 24-48 h restoring baseline; Joint cTn or CK-MB make up for a lack of specificity, avoid misdiagnosis in patients with skeletal muscle injury | ||||
| Biomarker | H-FABP | Full name | Heart-type fatty acid-binding protein | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | 15 kDa | Core Functional Dimensions | Early diagnosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, skeletal muscle (minor) | Test Sample / Technology Platform | Plasma (immune chromatography) | ||
| Pathobiological Mechanisms | Myocardial injury after the quick release (2 to 3 hours earlier than cTn), can fill the AMI super early detection blind area | ||||
| Clinical Availability Status | Validation: suitable for super early screening of AMI within 6 hours of symptom onset, auxiliary emergency triage quickly | ||||
| Notes and Dynamics | With cTn joint detection can promote the AMI early diagnosis sensitivity, especially for emergency patients symptoms are not typical | ||||
| Biomarker | Lp-PLA2 | Full name | Lipoprotein-associated phospholipase A2 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 45 kDa | Core Functional Dimensions | Susceptibility |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Liver, macrophages, platelets | Test Sample / Technology Platform | Plasma (ELISA) | ||
| Pathobiological Mechanisms | Hydrolysis, the oxidation of phospholipids in the arteries, the proinflammatory medium, accelerate the process of atherosclerosis, increase the risk of plaque rupture | ||||
| Clinical Availability Status | Validation/clinical exploration: specific reflect the inflammation of the blood vessel walls, is the key to predict plaque stability markers | ||||
| Notes and Dynamics | Different from systemic inflammation index, of atherosclerosis has specificity, is expected to be incorporated in the high-risk population screening for coronary heart disease system | ||||
| Biomarker | CRP | Full name | C-reactive protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 11.6 kDa | Core Functional Dimensions | Susceptibility, early diagnosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Liver | Test Sample / Technology Platform | Whole blood/plasma (immunoturbidimetry) | ||
| Pathobiological Mechanisms | Inflammation markers of atherosclerosis, promote plaque lipid deposition and degradation of fibrous cap, and increased plaque instability | ||||
| Clinical Availability Status | Clinical use/research validation: to predict the risk of coronary heart disease, evaluate the inflammatory activity of plaque, and assist in judging the progression of disease | ||||
| Notes and Dynamics | Hs-CRP joint lipid indicators (such as LDL-C) of coronary heart disease risk stratification model can be optimized, high-risk population recognition rate | ||||
| Biomarker | BNP/NT-proBNP | Full name | Brain natriuretic peptide / N-terminal pro-brain natriuretic peptide | Molecular Type | Peptides |
| Molecular Formula | / | Molecular Weight | BNP: 4 kDa; NT-proBNP: 10 kDa | Core Functional Dimensions | Prognosis, cardiac function evaluation |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium (ventricular cardiomyocytes) | Test Sample / Technology Platform | Whole blood plasma (immunofluorescence) | ||
| Pathobiological Mechanisms | Ventricular pressure load induced synthesis, reflect the degree of myocardial reconstruction and cardiac insufficiency severity | ||||
| Clinical Availability Status | Clinical routine: used for heart failure stratification and prognosis judgment, one of the core risk stratification indicators for ACS patients | ||||
| Notes and Dynamics | The stability of NT-proBNP is better than that of BNP, and its half-life is longer, which is more suitable for long-term follow-up monitoring of cardiac function changes | ||||
| Biomarker | BNP/NT-proBNP | Full name | Brain natriuretic peptide / N-terminal pro-brain natriuretic peptide | Molecular Type | Peptides |
| Molecular Formula | / | Molecular Weight | BNP: 4 kDa; NT-proBNP: 10 kDa | Core Functional Dimensions | Prognosis, cardiac function evaluation |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium (ventricular cardiomyocytes) | Test Sample / Technology Platform | Whole blood plasma (immunofluorescence) | ||
| Pathobiological Mechanisms | Ventricular pressure load induced synthesis, reflect the degree of myocardial reconstruction and cardiac insufficiency severity | ||||
| Clinical Availability Status | Clinical routine: used for heart failure stratification and prognosis judgment, one of the core risk stratification indicators for ACS patients | ||||
| Notes and Dynamics | The stability of NT-proBNP is better than that of BNP, and its half-life is longer, which is more suitable for long-term follow-up monitoring of cardiac function changes | ||||
| Biomarker | CK-MB | Full name | Creatine kinase MB isoenzyme | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 86 kDa | Core Functional Dimensions | Diagnosis, assessment of the condition |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, skeletal muscle (minor) | Test Sample / Technology Platform | Whole blood/plasma (immunoturbidimetry, mass spectrometry) | ||
| Pathobiological Mechanisms | Enzymes released after myocardial injury, level changes reflect infarction range, also can evaluate reperfusion therapeutic effect | ||||
| Clinical Availability Status | Clinical routine/validation: auxiliary cTn diagnosis, supplementary assess the degree of myocardial injury, especially for reperfusion efficacy monitoring | ||||
| Notes and Dynamics | Percutaneous coronary intervention (PCI) after 12 hours of CK-MB level, can accurately predict the forward area of myocardial infarction (MI), guiding the follow-up treatment | ||||
| Biomarker | CK-MB | Full name | Creatine kinase MB isoenzyme | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 86 kDa | Core Functional Dimensions | Diagnosis, assessment of the condition |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium, skeletal muscle (minor) | Test Sample / Technology Platform | Whole blood/plasma (immunoturbidimetry, mass spectrometry) | ||
| Pathobiological Mechanisms | Enzymes released after myocardial injury, level changes reflect infarction range, also can evaluate reperfusion therapeutic effect | ||||
| Clinical Availability Status | Clinical routine/validation: auxiliary cTn diagnosis, supplementary assess the degree of myocardial injury, especially for reperfusion efficacy monitoring | ||||
| Notes and Dynamics | Percutaneous coronary intervention (PCI) after 12 hours of CK-MB level, can accurately predict the forward area of myocardial infarction (MI), guiding the follow-up treatment | ||||
| Biomarker | cTnI/cTnT | Full name | Cardiac troponin I / Cardiac troponin T | Molecular Type | protein |
| Molecular Formula | / | Molecular Weight | cTnI: 24 kDa; cTnT: ~37 kDa | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium (cardiac muscle cells) | Test Sample / Technology Platform | Whole blood plasma (ECLIA and ELISA) | ||
| Pathobiological Mechanisms | Ischemic necrosis of the myocardium leads to rupture of cardiomyocytes and release of specific troponin into the blood. | ||||
| Clinical Availability Status | Clinical routine/guidelines recommend: acute myocardial infarction (AMI) in the diagnosis of gold standard, high-sensitivity detection can be early identification of myocardial injury | ||||
| Notes and Dynamics | Hs-cTn can realize AMI within 3 hours of symptom onset, rapid diagnostic core indicators is the emergency department, reduce missed diagnosis | ||||
| Biomarker | Complement C3 | Full name | Complement component 3 | Molecular Type | Proteins (complement components) |
| Molecular Formula | / | Molecular Weight | 187 kDa | Core Functional Dimensions | Susceptibility and prognosis |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Liver | Test Sample / Technology Platform | Serum/plasma (immunoturbidimetry, ELISA) | ||
| Pathobiological Mechanisms | Activate the complement system, involved in vascular inflammation, promote endothelial injury and vascular remodeling | ||||
| Clinical Availability Status | Clinically available/research validated: used for risk assessment of hypertension and associated with progression of blood pressure | ||||
| Notes and Dynamics | Complement C3 | ||||
| Biomarker | Adiponectin | Full name | Adiponectin | Molecular Type | Proteins (adipokines) |
| Molecular Formula | / | Molecular Weight | 30 kDa | Core Functional Dimensions | Susceptibility, prognosis |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Adipose tissue | Test Sample / Technology Platform | Serum/plasma (ELISA, mass spectrometry) | ||
| Pathobiological Mechanisms | It has anti-inflammatory and anti-atherosclerotic effects, and reduced levels can exacerbate vascular endothelial dysfunction and increase blood pressure | ||||
| Clinical Availability Status | Study validation: negative correlation with hypertension, used to assess the risk of metabolism-related hypertension | ||||
| Notes and Dynamics | Adiponectin levels are significantly decreased in obese and insulin resistant patients, and supplementation of adiponectin analogues can improve vascular function in experimental hypertension | ||||
| Biomarker | Leptin | Full name | Leptin | Molecular Type | Protein (fat factor) |
| Molecular Formula | / | Molecular Weight | 16 kDa | Core Functional Dimensions | Susceptibility, prognosis |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Adipose tissue | Test Sample / Technology Platform | Serum/plasma (ELISA, immunoradiometric assay) | ||
| Pathobiological Mechanisms | Obesity related fat factor, directly stimulate the adrenal aldosterone secretion, activation of the sympathetic nerve, promote water retention of sodium | ||||
| Clinical Availability Status | Validation/clinical exploration: closely associated with obesity related hypertension, used for risk stratification | ||||
| Notes and Dynamics | There is common in patients with obesity leptin resistance, but its cardiovascular effects persist, is an important intervention targets for obesity related hypertension | ||||
| Biomarker | ARR (Aldosterone/Renin Ratio) | Full name | Renin | Molecular Type | Protein (protease) |
| Molecular Formula | N/A (ratio) | Molecular Weight | 37 kDa | Core Functional Dimensions | Diagnosis, susceptibility, monitoring |
| Disease(or Constitution) | hypertension | Disease Subtypes | / | ||
| Organ | Kidney, adrenal cortex | Test Sample / Technology Platform | Serum/plasma (radioimmunoassay, ELISA, chemiluminescence) | ||
| Pathobiological Mechanisms | Reflect the degree of RAAS system imbalance, higher ratio of prompt aldosterone is relatively too much | ||||
| Clinical Availability Status | Clinically available (screening for primary aldosteronism) | ||||
| Notes and Dynamics | Is secondary hypertension etiology identification, especially the choice of primary aldosteronism screening tool, need to strictly control the conditions before testing | ||||