Protective role of NRF2 in macrovascular complications of diabetes.

Macrovascular complications develop in over a half of the diabetic individuals, resulting in high morbidity and mortality. This poses a severe threat to public health and a heavy burden to social economy. It is therefore important to develop effective approaches to prevent or slow down the pathogenesis and progression of macrovascular complications of diabetes (MCD). Oxidative stress is a major contributor to MCD. Nuclear factor (erythroid-derived 2)-like 2 (NRF2) governs cellular antioxidant defence system by activating the transcription of various antioxidant genes, combating diabetes-induced oxidative stress. Accumulating experimental evidence has demonstrated that NRF2 activation protects against MCD. Structural inhibition of Kelch-like ECH-associated protein 1 (KEAP1) is a canonical way to activate NRF2. More recently, novel approaches, such as activation of the Nfe2l2 gene transcription, decreasing KEAP1 protein level by microRNA-induced degradation of Keap1 mRNA, prevention of proteasomal degradation of NRF2 protein and modulation of other upstream regulators of NRF2, have emerged in prevention of MCD. This review provides a brief introduction of the pathophysiology of MCD and the role of oxidative stress in the pathogenesis of MCD. By reviewing previous work on the activation of NRF2 in MCD, we summarize strategies to activate NRF2, providing clues for future intervention of MCD. Controversies over NRF2 activation and future perspectives are also provided in this review.

Expression level and diagnostic value of exosomal NEAT1/miR-204/MMP-9 in acute ST-segment elevation myocardial infarction.

Acute myocardium infarction (AMI) is one of the main causes of cardiovascular death, and timely intervention and diagnosis are essential. Owing to the irreversible apoptosis and death of myocardial cells, which ultimately causes heart failure, the problem of myocardial repair after myocardial infarction needs to be urgently addressed. Exosomes can act as messengers between cells, delivering large amounts of proteins, RNA, and lipids to receptor cells, and regulating target cell functions. Studies have shown that exosomes can repair infarcted myocardium. We aimed to investigate the relationship between long non-coding RNA NEAT1 in serum exosomes of patients and AMI and its underlying mechanism. Subjects were divided into control, UA, and STEMI groups. RNA was extracted from the serum exosomes, and the expressions of lncRNA NEAT1 and miR-204 were detected by qRT-PCR. MMP-9 was detected by western blot, Spearman test was used to analyze the correlation among the three. Logistic regression and Receiver-operating characteristic curve (ROC) were used to evaluate the prediction of acute myocardial infarction. The expressions of NEAT1 and MMP-9 in serum exosomes of patients with acute ST-segment elevation myocardial infarction were up-regulated and positively correlated, miR-204 expression was down-regulated, there were no correlations between miR-204 with NEAT1, or MMP-9. Exosomal NEAT1, miR-204, and MMP-9 displayed potent biomarkers for diagnosis of acute ST-segment elevation myocardial infarction.

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.

Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylation, decreased microRNA-34a (miR-34a) level, leading to a dramatic increase in sirtuin 1 (SIRT1) protein level. Interestingly, the miR-34a inhibitor (miR-34a-I) and PFT-α increased SIRT1 protein level and alleviated the HG-induced endothelial inflammation and oxidative stress to a similar extent; however, these effects of PFT-α were completely abrogated by the miR-34a mimic. In addition, SIRT1 inhibition by EX-527 or Sirt1-siRNA completely abolished miR-34a-I's protection against HG-induced endothelial inflammation and oxidative stress. Furthermore, in the aortas of streptozotocin-induced diabetic mice, both PFT-α and miR-34a-I rescued the inflammation, oxidative stress and endothelial dysfunction caused by hyperglycaemia. Hence, the present study has uncovered a P53/miR-34a/SIRT1 pathway that leads to endothelial dysfunction, suggesting that P53/miR-34a inhibition could be a viable strategy in the management of diabetic macrovascular diseases.

Differences in the treatment and control of hypertension in urban and rural residents of the northeastern region of the People's Republic of China: a cross-sectional study.

BACKGROUND: Hypertension is a significant global public health problem and an important risk factor for cardiovascular diseases. We aimed to determine treatment and control rates of hypertension and to explore related risk factors by urban and rural areas. METHODS: A cross-sectional survey of 14,956 participants (≥ 15 years) was conducted in Jilin Province, China from July 2014 to December 2015 using questionnaire forms and physical measurements. RESULTS: Total rates of hypertension treatment, control, and controlled blood pressure among treated subjects were 31.7%, 8.8%, and 27.9% in the Jilin Province. Rates of hypertension treatment, control, and controlled blood pressure among treated subjects were 35.9%, 13.7%, and 38.3% in urban areas and 28.4%, 5.0%, and 17.5% in rural areas, respectively. Higher treatment of hypertension was associated with older age, female sex, other races (except Han), and higher body fat percentage in both areas. Among urban residents, higher education was additionally associated with higher treatment of hypertension; among rural residents, a family history of coronary artery disease and unemployment were associated with higher treatment of hypertension. Higher control of hypertension was associated with unemployment, married status, higher education, healthy body mass index, lower abdominal waist circumference, non-smoking status, and lower visceral adiposity index in urban residents; higher control of hypertension was associated with younger age in rural residents. CONCLUSION: Treatment and control rates of hypertension in urban and rural areas were lower than the national average; blood pressure control in patients taking antihypertensive drugs needs further improvement.

MicroRNA-210 Modulates the Cellular Energy Metabolism Shift During H2O2-Induced Oxidative Stress by Repressing ISCU in H9c2 Cardiomyocytes.

BACKGROUND/AIMS: The myocardial energy metabolism shift is one of the most important pathological features of ischemic heart disease (IHD). Although several microRNAs (miRs) are involved in the regulation of myocardial energy metabolism, their exact effects and underlying mechanisms remain unclear. The aim of this study was to investigate whether microRNA(miR-210) regulates the energy metabolism shift during oxidative stress in H9c2 cardiomyocytes. METHODS: Cell survival was analyzed via CCK assay. The energy metabolism shift was detected by lactate assay, ATP assay and RT2 profiler glucose metabolism PCR array. Protein and mRNA expression levels were determined by western blot and qPCR. We also used kits to detect the activity of Complex I, Sirt3 and the NAD+/NADH ratio. RESULTS: We determined that miR-210 promoted the energy metabolism shift. The iron-sulfur cluster assembly protein (ISCU) was a target of miR-210. Additionally, we detected the activity of complex I and found that miR-210 inhibits mitochondrial respiration. Interestingly, miR-210 may also indirectly regulate SIRT3 by regulating ISCU. CONCLUSION: Our results confirm that miR-210 is essential and sufficient for modulating the cellular energy metabolism shift during H2O2-induced oxidative stress in H9c2 cardiomyocytes by targeting ISCU.

Anti-apoptotic effect of microRNA-30b in early phase of rat myocardial ischemia-reperfusion injury model.

This study aimed to investigate the effect of microRNA-30b (miR-30b) in rat myocardial ischemic-reperfusion (I/R) injury model. We randomly divided Sprague-Dawley (SD) rats (n = 80) into five groups: 1) control group; 2) miR-30b group; 3) sham-operated group; 4) I/R group, and 5) I/R+miR-30b group. Real-time quantitative polymerase chain reaction, immunohistochemical staining and Western blot analysis were conducted. TUNEL assay was employed for testing cardiomyocyte apoptosis. Our results showed that miR-30b levels were down-regulated in I/R group and I/R + miR-30b group compared with sham-operated group (both P < 0.05). However, miR-30b level in I/R + miR-30b group was higher than I/R group (P < 0.05). Markedly, the apoptotic rate in I/R group showed highest in I/R group (P < 0.05). Additionally, the results illustrated that protein levels of Bcl-2, Bax, and caspase-3 were at higher levels in ischemic regions in I/R group, comparing to sham-operated group (all P < 0.05), while Bcl-2/Bax was reduced (P < 0.05). Bcl-2 level and Bcl-2/Bax were obviously increased in I/R + miR-30b group by comparison with I/R group, and expression levels of Bax and caspase-3 were down-regulated (all P < 0.05). We also found that in I/R + miR-30b group, KRAS level was apparently lower and p-AKT level was higher by comparing with I/R group (both P < 0.05). Our study indicated that miR-30b overexpression had anti-apoptotic effect on early phase of rat myocardial ischemia injury model through targeting KRAS and activating the Ras/Akt pathway.

MicroRNA-137 Negatively Regulates H2O2-Induced Cardiomyocyte Apoptosis Through CDC42.

BACKGROUND: Oxidative stress, inducing cardiomyocyte apoptosis or myocardial ischemia, is the major denominator of many cardiac diseases. In this study, we intended to explore the regulatory function of microRNA-137 (miR-137) in oxidative stress-induced cardiomyocyte apoptosis. MATERIAL AND METHODS: Cardiomyocytes were extracted from newborn C57BL/6 mice and cultured in vitro. Apoptosis was induced by H2O2, and evaluated by TUNEL assay. The effect of cardiomyocyte apoptosis on gene expression of miR-137 was evaluated by qRT-PCR. Lentivirus was used to stably down-regulate miR-137, and the subsequent effects of miR-137 down-regulation on cardiomyocyte apoptosis, its targeted gene CDC42, and caspase pathway were evaluated by TUNEL assay, dual-luciferase reporter assay, and Western blot assay, respectively. Finally, CDC42 was down-regulated by siRNA and its effect on miR-137-mediated cardiomyocyte apoptosis protection was examined. RESULTS: H2O2 induced significant apoptosis and up-regulated miR-137 in cardiomyocytes, whereas lentivirus-mediated miR-137 down-regulation protected against apoptosis. CDC42 was the direct target gene of miR-137 and proteins of CDC42, caspase-3, and caspase-9 were all regulated by miR-137 down-regulation in cardiomyocyte apoptosis. SiRNA-mediated CDC42 down-regulation reversed the protection of miR-137 down-regulation against cardiomyocyte apoptosis. CONCLUSIONS: Our work demonstrated miR-137 and CDC42 are critical regulators in cardiomyocyte apoptosis. It may help to identify the molecular targets to prevent myocardial injury in human patients.

Gut microbiota: a potential new regulator of hypertension.

Hypertension is a significant risk factor for cardiovascular and cerebrovascular diseases and has become a global public health concern. Although hypertension results from a combination of factors, the specific mechanism is still unclear. However, increasing evidence suggests that gut microbiota is closely associated with the development of hypertension. We provide a summary of the composition and physiological role of gut microbiota. We then delve into the mechanism of gut microbiota and its metabolites involved in the occurrence and development of hypertension. Finally, we review various regimens for better-controlling hypertension from the diet, exercise, drugs, antibiotics, probiotics, and fecal transplantation perspectives.

Metabolomics analysis of the nutraceutical diversity and physiological quality of Torreya yunnanensis seeds during cold storage.

This study investigated how cold storage affects the nutraceutical diversity and physiological quality of Torreya yunnanensis seeds, using a widely targeted UPLC-MS/MS-based metabolomics analysis. The 373 identified metabolites were divided into nine categories: lipids, phenolic acids, amino acids and derivatives, organic acids, nucleotides, saccharides, vitamins and alcohols. Among them, 49 metabolites showed significant changes after 3 months of cold storage, affecting 28 metabolic pathways. The content of amino acid-related metabolites significantly increased, while the content of sugar-related metabolites decreased during storage. Notably, the content of proline acid, shikimic acid, α-linolenic acid and branched-chain amino acids showed significant changes, indicating their potential role in seed storage. This study deepens our understanding of the nutraceutical diversity and physiological quality of T. yunnanensis seeds during storage, providing insight for conservation efforts and habitat restoration.

Ferroptosis: a new strategy for cardiovascular disease.

Cardiovascular disease (CVD) is currently one of the prevalent causes of human death. Iron is one of the essential trace elements in the human body and a vital component of living tissues. All organ systems require iron for various metabolic processes, including myocardial and skeletal muscle metabolism, erythropoiesis, mitochondrial function, and oxygen transport. Its deficiency or excess in the human body remains one of the nutritional problems worldwide. The total amount of iron in a normal human body is about 3-5 g. Iron deficiency may cause symptoms such as general fatigue, pica, and nerve deafness, while excessive iron plays a crucial role in the pathophysiological processes of the heart through ferroptosis triggered by the Fenton reaction. It differs from other cell death modes based on its dependence on the accumulation of lipid peroxides and REDOX imbalance, opening a new pathway underlying the pathogenesis and mechanism of CVDs. In this review, we describe the latest research progress on the mechanism of ferroptosis and report its crucial role and association with miRNA in various CVDs. Finally, we summarise the potential therapeutic value of ferroptosis-related drugs or ferroptosis inhibitors in CVDs.

[Chloroplast genomic characterization and phylogenetic analysis of Castanopsis hystrix].

The structure and size of the chloroplast genome of Castanopsis hystrix was determined by Illumina HiSeq 2500 sequencing platform to understand the difference between C. hystrix and the chloroplast genome of the same genus, and the evolutionary position of C. hystrix in the genus, so as to facilitate species identification, genetic diversity analysis and resource conservation of the genus. Bioinformatics analysis was used to perform sequence assembly, annotation and characteristic analysis. R, Python, MISA, CodonW and MEGA 6 bioinformatics software were used to analyze the genome structure and number, codon bias, sequence repeats, simple sequence repeat (SSR) loci and phylogeny. The genome size of C. hystrix chloroplast was 153 754 bp, showing tetrad structure. A total of 130 genes were identified, including 85 coding genes, 37 tRNA genes and 8 rRNA genes. According to codon bias analysis, the average number of effective codons was 55.5, indicating that the codons were highly random and low in bias. Forty-five repeats and 111 SSR loci were detected by SSR and long repeat fragment analysis. Compared with the related species, chloroplast genome sequences were highly conserved, especially the protein coding sequences. Phylogenetic analysis showed that C. hystrix is closely related to the Hainanese cone. In summary, we obtained the basic information and phylogenetic position of the chloroplast genome of red cone, which will provide a preliminary basis for species identification, genetic diversity of natural populations and functional genomics research of C. hystrix.

Krill Oil Inhibits NLRP3 Inflammasome Activation in the Prevention of the Pathological Injuries of Diabetic Cardiomyopathy.

Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of DCM. In the present study, we investigate the effect of krill oil (KO) on the prevention of DCM using a mouse model of DM induced by streptozotocin and a high-fat diet. The diabetic mice developed pathological features, including cardiac fibrosis, apoptosis and inflammatory cell infiltration, the effects of which were remarkably prevented by KO. Mechanistically, KO reversed the DM-induced cardiac expression of profibrotic and proinflammatory genes and attenuated DM-enhanced cardiac oxidative stress. Notably, KO exhibited a potent inhibitory effect on NLR family pyrin domain containing 3 (NLRP3) inflammasome that plays an important role in DCM. Further investigation showed that KO significantly upregulated the expression of Sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which are negative regulators of NLRP3. The present study reports for the first time the preventive effect of KO on the pathological injuries of DCM, providing SIRT3, PGC-1α and NLRP3 as molecular targets of KO. This work suggests that KO supplementation may be a viable approach in clinical prevention of DCM.

Acute myocardial infarction in the elderly with anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA): A case report and literature review.

INTRODUCTION: Anomalous left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital coronary artery malformation, with a fatality rate of 90% at 1 year of age; only 10% to 15% of patients are diagnosed in adulthood. However, elderly survivors are particularly rare. Here, we report a case of elderly ALCAPA presented with acute myocardial infarction. CASE PRESENTATION: A 64-years-old female, complained of acute precordial pain in our hospital for 2 days. She was diagnosed with an acute non-ST-segment elevation myocardial infarction. Aortic angiography revealed emptiness of the left coronary sinus, and coronary angiography showed that the tortuous right coronary artery supplied blood to the left coronary artery through collateral circulation, and the contrast medium spilled from the opening of the left coronary artery. It was suspected that the left coronary artery was opened in the pulmonary artery. This finding was subsequently confirmed by coronary artery CT. The patient refused surgery to restore double coronary circulation and was administered standardized drug treatment. There was no chest pain during the 6-month follow-up. CONCLUSION: ALCAPA should be considered in patients with Myocardial Infarction with Non-obstructive Coronary Arteries, and surgical intervention is the first choice for such patients; However, chronic myocardial damage persists regardless of surgical treatment, prophylactic implantation of an ICD may be an important means of preventing sudden cardiac death and such patients should be followed up for a lifetime.

Comparison of effectiveness and safety of high-power vs. conventional-power radiofrequency ablation for treatment of atrial fibrillation.

Aim: To compare high-power (HP) vs. conventional-power (CP) radiofrequency ablation for atrial fibrillation (AF). Methods: We retrospectively enrolled AF patients undergoing CP (30-40 W, 43 patients) or HP (50 W, 49 patients) radiofrequency ablation. Immediate pulmonary vein (PV) single-circle isolation, PV-ablation time, AF recurrence, AF recurrence-free survival, and complications were analyzed. Results: Diabetes was more common in the CP group than in the HP group (27.91% vs. 10.20%, P = 0.029). The left PV single-circle isolation rate (62.79% vs. 65.31%), right PV single-circle isolation rate (48.84% vs. 53.06%), and bilateral PV single-circle isolation rate (32.56% vs. 38.78%; all P > 0.05) did not differ between the groups. Single-circle ablation times for the left PVs (12.79 ± 3.39 vs. 22.94 ± 6.39 min), right PVs (12.18 ± 3.46 vs. 20.67 ± 5.44 min), and all PVs (25.85 ± 6.04 vs. 45.66 ± 11.11 min; all P < 0.001) were shorter in the HP group. Atrial fibrillation recurrence within 3 months (13.95% vs. 18.37%), at 3 months (11.63% vs. 8.16%), and at 6 months after ablation (18.60% vs. 12.24%; all P > 0.05) was similar in both groups. Atrial fibrillation recurrence-free survival did not differ between the groups (Kaplan-Meier analysis). Cardiac rupture and pericardial tamponade did not occur in any patient. Pops occurred in 2 and 0 patients in the HP and CP groups, respectively (4.08% vs. 0.00%, P = 0.533). Conclusion: High-power ablation improved operation time and efficiency without increasing complications.

Role of N6-Methyladenosine RNA Modification in Cardiovascular Disease.

Despite treatments being improved and many risk factors being identified, cardiovascular disease (CVD) is still a leading cause of mortality and disability worldwide. N6-methyladenosine (m6A) is the most common, abundant, and conserved internal modification in RNAs and plays an important role in the development of CVD. Many studies have shown that aabnormal m6A modifications of coding RNAs are involved in the development of CVD. In addition, non-coding RNAs (ncRNAs) exert post-transcriptional regulation in many diseases including CVD. Although ncRNAs have also been found to be modified by m6A, the studies on m6A modifications of ncRNAs in CVD are currently lacking. In this review, we summarized the recent progress in understanding m6A modifications in the context of coding RNAs and ncRNAs, as well as their regulatory roles in CVD.

Protocol for the Acute Myocardial Infarction Study in Northeastern China (AMINoC): a real-world prospective cohort study.

INTRODUCTION: Acute myocardial infarction (AMI) has become one of the major causes of mortality and morbidity in China. However, little is known about the characteristics, medical care and outcomes of patients with AMI in Northeastern China. The Acute Myocardial Infarction Study in Northeastern China (AMINoC) is aimed at obtaining timely real-world knowledge in terms of characteristics, clinical care and outcomes of patients with AMI and at providing care-quality improvement efforts in Northeastern China. METHODS AND ANALYSIS: The AMINoC is a real-world, prospective, multicentre cohort study. The study selected 20 hospitals using stratified cluster sampling from different levels of hospitals among nine districts throughout Jilin Province. Hospitalised patients with a primary diagnosis of AMI in each site are consecutively enrolled for 1 year. Demographic characteristics, clinical data, treatments, outcomes and cost are collected by local investigators. Patient follow-up after discharge is planned for up to 2 years. ETHICS AND DISSEMINATION: The protocol has been approved by the ethics committee at the Second Hospital of Jilin University. The findings of this study will be published in peer-reviewed journals and medical conferences. TRIAL REGISTRATION: NCT04451967.

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis.

Atherosclerosis is characterized as a chronic inflammatory response to cholesterol deposition in arteries. Low-density lipoprotein (LDL), especially the oxidized form (ox-LDL), plays a crucial role in the occurrence and development of atherosclerosis by inducing endothelial cell (EC) dysfunction, attracting monocyte-derived macrophages, and promoting chronic inflammation. However, the mechanisms linking cholesterol accumulation with inflammation in macrophage foam cells are poorly understood. Long non-coding RNAs (lncRNAs) are a group of non-protein-coding RNAs longer than 200 nucleotides and are found to regulate the progress of atherosclerosis. Recently, many lncRNAs interfering with cholesterol deposition or inflammation were identified, which might help elucidate their underlying molecular mechanism or be used as novel therapeutic targets. In this review, we summarize and highlight the role of lncRNAs linking cholesterol (mainly ox-LDL) accumulation with inflammation in macrophages during the process of atherosclerosis.

The Role of Exosomal Non-Coding RNAs in Coronary Artery Disease.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide. Atherosclerosis (AS) is a major cause of CVD. Oxidative stress, endothelial dysfunction, and inflammation are key factors involved in the development and progression of AS. Exosomes are nano-sized vesicles secreted into the extracellular space by most types of cells, and are ideal substances for the transmission and integration of signals between cells. Cells can selectively encapsulate biologically active substances, such as lipids, proteins and RNA in exosomes and act through paracrine mechanisms. Non-coding RNAs (ncRNAs) are important for communication between cells. They can reach the recipient cells through exosomes, causing phenotypic changes and playing a molecular regulatory role in cell function. Elucidating their molecular mechanisms can help identify therapeutic targets or strategies for CVD. Coronary artery disease (CAD) is the most important disease in CVD. Here, we review the role and the regulatory mechanism of exosomal ncRNAs in the pathophysiology of CAD, as well as the potential contribution of exosomal ncRNA to diagnosis and treatment of CAD.

Coronary sequelae of Kawasaki disease treated with rotational atherectomy and drug coated balloon: A case report.

INTRODUCTION: Kawasaki disease (KD) is an acute vasculitis syndrome that mainly affects children and is the first cause of acquired heart disease. Coronary artery lesion is the most serious complication of KD. Only two previous studies have reported similar cases, but we reported patient was younger and had a longer follow-up. PATIENT CONCERNS: We reported a case of coronary sequelae of KD treated with rotational atherectomy and drug coated balloon (DCB). During the week after surgery, the patient complained of a slight chest pain intermittently, but no longer appeared after that. DIAGNOSIS: We diagnosed by electrocardiogram and angiography. Angiography showed that the anterior descending branch (LAD) proximal stenosis was 95%, the right coronary artery (RCA) middle stenosis was 99%, and the calcification was severe. INTERVENTIONS: We treat the patient with rotational atherectomy using a 1.25 mm burr, pre-dilatation of the stenosis lesion with a 3.5 mm × 15 mm non-compliant balloon was achieved. Then 3.5 mm × 15 mm drug eluting balloon was inflated at 10 atm for 60 seconds. OUTCOMES: After the 6-month follow-up (from October 2018 to March 2019), the symptom of angina disappeared. Coronary angiography 6 months later showed no apparent progression of vessel narrowing. CONCLUSION: The present case suggests that rotational atherectomy followed by DCB dilation could be an alternative revascularization therapy of choice in coronary KD sequelae complicated with atherosclerosis.

Awareness of hypertension and related factors in northeastern China: a cross-sectional study.

Timely awareness of hypertension is among the most crucial components in reducing the burden of hypertension. However, there is limited information about the awareness of hypertension in northern China. Therefore, in this cross-sectional study, we aimed to investigate the awareness of hypertension and its associated factors in the Jilin province in China; the study was conducted between July 2014 and December 2015 in four cities and four rural counties in the Jilin province as part of a national study. A stratified multistage random-sampling method was used to select a representative sample: a total of 15,206 participants aged ≥15 years were initially recruited, among which 14,956 were finally included in the survey. The awareness of hypertension in the Jilin province was found to be 42.3%. Moreover, the awareness of hypertension was associated with age, sex, region, marital status, body mass index, and family history of hypertension or coronary artery disease. Employment was associated with a lower awareness in rural areas, whereas high education was associated with a higher awareness in urban areas. Policies targeting specific subgroups may be helpful in increasing the awareness of hypertension in the Jilin province.