Background:Cystatin C (CysC), a low-molecular-weight protein, is widely used as a biomarker of renal function. The relationship between CysC and cognitive impairment remains controversial. This study aimed to investigate the association between CysC and cognitive impairment in the Hanzhong Adolescent Hypertension Study. Methods:A total of 2,347 participants completed the Mini-Mental State Examination (MMSE) in 2023, after excluding the participants missing data, 1929 participants were included. Multivariable logistic regression was used to assess the cross-sectional association between serum CysC levels and cognitive impairment. Subgroup and interaction analyses were performed to examine effect modification by albuminuria status. The nonlinear relationship was explored using restricted cubic splines (RCS). Results:Cognitive impairment was identified in 149 participants (7.72%). Each 1-SD increase in CysC levels was significantly associated with 49% higher odds of cognitive impairment after full adjustment [odds ratio (OR) = 1.49, 95% confidence interval (CI): 1.24-1.79, p < 0.001]. Compared with participants in the lowest CysC quartile, those in the highest quartile had significantly higher odds of cognitive impairment (OR = 1.79, 95% CI = 1.09-2.98, p = 0.022). The association was stronger in participants without albuminuria (OR per SD = 1.48, 95% CI: 1.22-1.80, p < 0.001) but absent in those with albuminuria (OR per SD = 1.00, 95% CI: 0.73-1.25, p = 0.981), with a significant interaction when CysC was modeled continuously (p for interaction = 0.028). A linear and positive association was observed between cystatin C levels and the prevalence of cognitive impairment (p for linearity < 0.001). This association remained significant in the non-albuminuria subgroup. Conclusion:Elevated CysC is associated with cognitive impairment assessed by MMSE in this midlife natural population cohort. This association is stronger in participants without albuminuria.

The sensitive period during which the adult cardiovascular system is particularly vulnerable to body mass index (BMI) changes remains unclear. This study aimed to examine how rates of BMI change from childhood to adulthood influence the risk of subclinical cardiovascular outcomes in mid-adulthood. This cohort study included 2446 participants from the Hanzhong Adolescent Hypertension Study who had at least two BMI measurements in childhood/adolescence (6–18 years) and at least two in adulthood (≥ 19 years). The BMI growth curve from ages 6 to 52 years was modeled using random-effects mixed models with restricted cubic splines. These models yielded age-specific estimates of BMI levels and rates of change, the latter of which were subsequently residual-adjusted for concurrent BMI levels. Multivariable logistic regression models were used to examine the associations of BMI levels and level-adjusted rates of change from 6 to 52 years with left ventricular hypertrophy (LVH) and arterial stiffness in mid-adulthood. BMI at each age from 10 to 52 years was associated with mid-adult LVH and arterial stiffness, and these associations became stronger with increasing age at BMI measurement. Additionally, age-level–adjusted rates of BMI change at most ages from childhood to adulthood were positively associated with a higher risk of both subclinical cardiovascular outcomes. However, the odds ratios (ORs) for both LVH and arterial stiffness per 1-SD increase in BMI change rate declined with increasing age. For LVH, the ORs decreased from 2.49 (95

Insulin resistance promotes both arterial stiffening and carotid atherosclerosis, but the comparative value of TyG-related indices for these phenotypes is unclear. Using a cohort with childhood anthropometry measured in 1987, we compared two vascular phenotypes, functional arterial stiffness (AS) and structural carotid intima–media thickening (cIMT), in relation to a common metabolic exposure, tested independence from early-life adiposity, and examined how the choice of exposure design (baseline, cumulative, or change) shaped these associations. Within the Hanzhong Adolescent Hypertension Cohort (established 1987), we analysed 1,294 (incident AS) and 1,408 (incident cIMT) adults free of the respective outcome in 2017 and re-examined in 2023. Eight indices (TyG, TyG-BMI, TyG-WC, TyG-WHtR, TyG-WWI, TyG-BRI, TyG-CVAI, METS-IR) were modelled as baseline, cumulative, and 6-year change exposures. Incident AS was defined as brachial–ankle pulse wave velocity ≥ 1,400 cm/s, and incident cIMT thickening as mean cIMT ≥ 0.9 mm. Logistic regression, restricted cubic splines, and discrimination/reclassification metrics were applied, with additional adjustment for childhood (1987) BMI Z-score. Over 6 years, 296 (22.9

Objective To examine the associations between cumulative body mass index (BMI) burden from childhood to adulthood and the risk of adult metabolic multimorbidity. Research Design and Methods This prospective cohort study used data from the Hanzhong Adolescent Hypertension Study (1987-2023). A total of 2,446 participants with at least two BMI measurements in both childhood (6-18 years) and adulthood (19-52 years) were included. Cumulative BMI exposure was quantified using total and incremental area under the curve (AUC). Outcomes included metabolic multimorbidity, defined as the presence of ≥2 or ≥3 metabolic diseases, specifically hypertension, diabetes, dyslipidemia, elevated liver enzymes/bilirubin, and kidney damage. Results Higher total and incremental BMI AUC during childhood, adulthood, and over the life course were consistently associated with an increased risk of adult metabolic multimorbidity (≥2 diseases). For total AUC, odds ratios (ORs) ranged from 1.51 to 2.59 (all P<0.05); for incremental AUC, ORs ranged from 1.94 to 4.33 (all P<0.05). Compared with total AUC, incremental AUC showed a stronger association with metabolic multimorbidity in childhood (OR: 4.33, 95%CI: 2.93-6.40 vs. 1.51, 1.17-1.95, respectively). Conversely, total AUC exhibited a stronger association in adulthood than in childhood (OR: 2.51, 95%CI: 2.08-3.04 vs. 1.94, 1.62-2.31). Furthermore, the associations for adulthood and life-course BMI AUC were significantly stronger in males than in females (P for interaction <0.05). Conclusions These findings highlight the importance of life stage-specific strategies: curbing rapid BMI gain in childhood and maintaining long-term weight control throughout adulthood.

BACKGROUND:Blood pressure (BP) is a dynamic trait associated with cardiovascular disease. We aimed to estimate age-specific BP levels and rates of change from childhood to mid-adulthood and to examine their associations with subsequent subclinical target organ damage. METHODS:We included 2508 participants from the Hanzhong Adolescent Hypertension Study with BP measured ≥4× from 1987 to 2023. Surrogate markers of target organ damage were assessed, including arterial stiffness, left ventricular hypertrophy, and albuminuria. Growth models were used to construct BP trajectories and estimate age-specific BP levels and rates of change (slopes). RESULTS:Rates of change in BP at each age point from childhood to mid-adulthood were positively associated with arterial stiffness and albuminuria in mid-adulthood, independent of corresponding BP levels. The magnitude of the associations rose from childhood, peaked in adolescence, and declined thereafter. For example, odds ratios (95% CIs) per 1 SD increase in systolic BP change rates for arterial stiffness increased from 1.94 (1.69-2.24) at age 6 to 2.11 (1.82-2.44) at age 13, then declined to 1.13 (1.01-1.28) by age 52. Faster BP increases were more strongly associated with arterial stiffness and albuminuria than concurrent BP levels during childhood and adolescence, whereas the opposite trend was observed in young and mid-adulthood. Similar age-dependent trends were identified for left ventricular hypertrophy, with minor variations in the ages at which associations reached statistical significance. CONCLUSIONS:Accelerated BP increases during childhood and adolescence show a stronger association with mid-adult subclinical target organ damage than increases occurring in adulthood.

Aims: This study aims to characterize the heterogeneity of the cardiovascular-kidney-liver-metabolic (CKLM) spectrum and to assess the independent, synergistic, and competitive effects of liver fibrosis risk (FIB-4 index) and cardiovascular-kidney-metabolic (CKM) risk on mortality. Methods: This study included 28,056 U.S. adults from the NHANES (2005-2016) with a median follow-up of 9.08 years. Using Cox proportional hazards regression, restricted cubic splines, and sensitivity analyses, the primary analysis evaluated the associations of composite heterogeneous phenotypes—defined by CKM stage (low-risk: 0-2; high-risk: 3-4) and FIB-4 index (low, intermediate, high)—with all-cause and cardiovascular mortality. Results: In the community-based population, detectable liver disease risk often precedes CKM risk and affects a broader population. Among the five high-risk heterogeneous phenotypes (collectively 31.2%), the "CKM-low/FIB-4-intermediate" phenotype was the most prevalent (16.2%), carried a significant mortality risk, and increased over the study period. The "CKM-low/FIB-4-high" phenotype (1.4%) represents a cardiometabolically healthy but high-mortality-risk phenotype. Compared to the dual-low-risk phenotype (68.8%), the dual-high-risk phenotype (1.3%) was associated with a 621% (HR=7.21) and a 1307% (HR=14.07) increase in all-cause and cardiovascular mortality risk, respectively. Individually, elevated FIB-4 conferred similar magnitudes of increased risk for all-cause and cardiovascular mortality, whereas elevated CKM conferred a cardiovascular mortality risk increase approximately twice that of all-cause mortality. A competitive risk interaction was observed: the hazard ratio (HR) for all-cause mortality associated with an increase in FIB-4 from low to high was 5.29 in the CKM-low group, compared to 2.98 in the CKM-high group. Among individuals with high FIB-4 risk, further progression from low to high CKM risk did not contribute additional mortality risk. Conclusions: Liver fibrosis risk (FIB-4 index) and CKM stage independently, synergistically, and competitively increase mortality risk. Their combined stratification identified six heterogeneous CKLM phenotypes, increasing the proportion of the population identified as high-risk from 13.6% (using CKM alone) to 31.2%, thereby achieving more precise risk stratification.KeywordsCKM syndrome​, FIB-4 index​, Liver fibrosis​, All-cause mortality​, Cardiovascular mortality​, Risk stratification

The associations of long-term body mass index (BMI) exposure, including both cumulative burden and increasing trends from childhood to adulthood, with subclinical cardiovascular outcomes remain incompletely understood, especially across distinct life stages. This study aimed to examine these associations and evaluate the potential mediating roles of established cardiovascular risk factors. We analyzed data from 2,446 participants in the Hanzhong Adolescent Hypertension Study, all of whom had at least four BMI measurements over a 36-year follow-up period. Cumulative burden and increasing trends of BMI were quantified using total and incremental areas under the curve (AUCs). Multivariable logistic regression and exploratory multiple-mediator analyses were used to examine associations and potential indirect-effect patterns, respectively. Higher total and incremental BMI AUCs during childhood, adulthood, and across the life course were significantly associated with an increased risk of arterial stiffness in mid-adulthood. For childhood, the odds ratios (ORs) with 95

The TKI-targeted agent lapatinib has been applied in clinical oncology for the management of multiple malignancies. Nonetheless, its therapeutic benefit is restricted by cardiotoxic effects that endanger patient survival, and the underlying molecular basis remains unclear. The GSE146096 dataset containing transcriptomic profiles of lapatinib-exposed human cardiomyocytes was analyzed to identify ferroptosis-related differentially expressed genes (DEGs). Protein expression of selected targets was subsequently confirmed by Western Blot. Reactive oxygen species (ROS) accumulation, Fe²⁺ levels, and mitochondrial membrane potential in AC16 cells exposed to lapatinib were examined using confocal microscopy. A microplate reader was employed to quantify alterations in malondialdehyde (MDA) and glutathione (GSH) levels in cardiomyocytes. Eight ferroptosis-associated genes were identified in lapatinib-treated cardiomyocytes, including the canonical regulator GPX4. siRNA interference and Western Blot analyses demonstrated marked induction of ATF4 expression and significant suppression of GPX4 expression following lapatinib exposure in AC16 cells. CCK-8 assays indicated dose-dependent cytotoxicity. Confocal microscopy and transmission electron microscopy (TEM) revealed altered mitochondrial morphology accompanied by a reduction in mitochondrial membrane potential. Intracellular MDA levels increased substantially, whereas GSH levels declined, indicating lipid peroxidation and subsequent ferroptosis. Treatment with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) or silencing of ATF4 expression effectively attenuated lapatinib-induced cytotoxicity. Lapatinib enhances ATF4 expression in cardiomyocytes, suppresses GPX4, triggers lipid peroxidation, induces ferroptosis, and thereby contributes to cardiotoxicity.

OBJECTIVE:We investigated the associations between BMI transitions from childhood to adulthood and cardiovascular-kidney-metabolic (CKM) syndrome and its components in midlife. RESEARCH DESIGN AND METHODS:Using data from the Hanzhong Adolescent Hypertension Study, 1,997 participants aged 6-18 years were followed for 36 years into midlife (mean age 48.12 years). Participants were categorized into four groups based on BMI transitions from childhood to midlife: control, incident, persistent, and resolution. CKM stages ranged from early (stages 0-1), to intermediate (stage 2), to advanced (stages 3-4), defined by cardiovascular disease, chronic kidney disease, and metabolic disorders. Multivariable regression models were used to assess associations between BMI transitions and CKM outcomes. RESULTS:Individuals transitioning from normal childhood BMI to overweight in adulthood had higher risks of intermediate (odds ratio [OR] 5.19 [95% CI 3.15-8.53]) and advanced CKM stages (OR 6.70 [95% CI 3.96-11.33]) compared with those with persistently normal BMI. These risks were attenuated if elevated childhood BMI resolved by adulthood. For specific CKM components, individuals with normal childhood BMI but overweight in adulthood showed higher risks of left ventricular diastolic dysfunction, subclinical kidney damage, albuminuria, and metabolic abnormalities compared with those with persistently normal BMI. These risks were reduced if high childhood BMI normalized by adulthood. CONCLUSIONS:Transitioning from normal childhood BMI to overweight in adulthood is associated with increased risks of higher CKM stages in midlife. However, individuals whose high childhood BMI resolved by adulthood exhibit similar risk to those with persistently normal BMI.

Background: The link between chronic non-communicable diseases (NCDs) and poverty in underdeveloped countries is debated. This study aims to examine socioeconomic inequalities related to NCDs and assess the contributing factors to these disparities. Methods: The study utilized data from the National Health Services Survey in Shaanxi Province for 2003, 2008, and 2013, having 71,766 respondents. The concentration index (CI) was employed to rigorously quantify the degree of socioeconomic inequality in the prevalence of non-communicable diseases (NCDs). The CI decomposition identified the contribution of each variable, while the horizontal inequity (HI) index was calculated annually to assess changes in inequality. Additionally, a Probit model was employed to examine the significant determinants contributing to the occurrence of NCDs. Results: The results show a significant increase in NCD prevalence with age, particularly for individuals aged 60 and above, who experienced a 286.55% rise from 2003 to 2013. Higher education levels are associated with decreased NCD prevalence, as evidenced by a 74.13% reduction for those with high school education or above. Additionally, wealthier individuals had a 15.31% lower prevalence of NCDs, indicating that higher socioeconomic status correlates with a reduced likelihood of chronic diseases. Conclusions: The study finds that NCD prevalence significantly increases with age, while higher education levels and greater wealth are associated with reduced prevalence. These findings highlight the need to target older populations and lower socioeconomic groups for effective NCD prevention and management. Policies should focus on improving educational opportunities and socioeconomic conditions to reduce the burden of NCDs, particularly among older and economically disadvantaged groups.

Background Elevated blood pressure (BP) in childhood is associated with adult hypertension and arterial stiffness. However, the effect of long-term time in target range (TTR) for BP since childhood on the risk of arterial stiffness in midlife remains unclear. Objectives The purpose of this study was to determine the independent association of TTR for systolic blood pressure (SBP) from childhood to midlife with arterial stiffness in adulthood. Methods This study used data from the ongoing cohort of the Hanzhong Adolescent Hypertension Study. SBP-TTR was assessed over 36 years, with the target ranges of SBP defined as the 90th to 95th percentile of SBP for age, sex, and height in childhood, and 110 to 130 mm Hg in adulthood. Arterial stiffness was defined as brachial-ankle pulse wave velocity >1,400 cm/s. Results Of the total 1,959 participants, 55.5% (1,088 of 1,959) were men, and the mean age was 49 years. The risk of arterial stiffness exhibited a gradual decrease with increasing SBP-TTR over the 36-year follow-up. Compared with the participants in the lowest quartile of SBP-TTR from childhood to midlife, those in the highest quartile showed significantly reduced arterial stiffness risk in midlife. This association persisted even after adjusting for mean SBP and SBP variability. Furthermore, men in the highest quartile of SBP-TTR demonstrated a markedly lower arterial stiffness risk than those in the lowest quartile, whereas this effect was not observed in women. Conclusions Higher long-term SBP-TTR from childhood to midlife is associated with a reduced risk of arterial stiffness in midlife, regardless of the mean SBP or SBP variability.

Dysregulated energy metabolism, particularly lipid metabolism disorders, has been identified as a key factor in the development of diabetic cardiomyopathy (DCM). Sirtuin 2 (SIRT2) is a deacetylase involved in the regulation of metabolism and cellular energy homeostasis, yet its role in the progression of DCM remains unclear. We observed significantly reduced SIRT2 expression in DCM model mice. Cardiac-specific overexpression of SIRT2 protected mice from streptozotocin/high-fat diet (STZ/HFD)-induced insulin resistance (IR), cell apoptosis, and cardiac dysfunction, whereas its downregulation exacerbated these conditions. Moreover, we found that SIRT2 regulated cardiac lipid accumulation and fatty acid oxidation (FAO), and identified its localization in cardiac mitochondria. Mechanistically, we determined carnitine palmitoyltransferase 2 (CPT2) as a critical substrate of SIRT2, which is implicated in DCM. SIRT2-mediated deacetylation at K239 enhanced CPT2 ubiquitination, resulting in decreased protein stability and subsequent inhibition of FAO and reactive oxygen species (ROS) production. Taken together, these findings suggest that the SIRT2/CPT2 signaling pathway plays a crucial role in DCM progression.

Objective: Elevated blood pressure (BP) in childhood is associated with adult hypertension and arterial stiffness. We aimed to determine the independent association of time in target range (TTR) for systolic blood pressure (SBP) from childhood to midlife with arterial stiffness in midlife. Design and method: Using data from the ongoing cohort of Hanzhong Adolescent Hypertension study, 1959 children and adolescents aged 6 to 18 years were enrolled at baseline. We assessed SBP-TTR from childhood to adulthood for 36 years, with the target range of SBP defined as 90th – 95th percentile for age, sex, and height in childhood, and 110 to 130 mmHg in adulthood. Results: During the 36 years of follow-up, the risk of arterial stiffness gradually decreased with increasing TTR for SBP. After fully adjustment for traditional cardiovascular risk factors, comparing the highest vs. lowest quartiles of TTR for SBP, the odds ratios (ORs) [95% confidence intervals (CIs)] were 0.642 (0.452-0.911) for the risk of arterial stiffness in adulthood. TTR remained significantly associated with arterial stiffness despite adjustment for mean SBP or SBP variability. In addition, males with highest quartile of SBP-TTR was significantly associated with a decreased risk of arterial stiffness [OR 95% CI, 0.432 (0.262-0.710)], while no significant difference was found in females compared with the lowest TTR group. Conclusions: Higher long-term TTR for SBP from childhood to adulthood was associated with a decreased risk of arterial stiffness in adulthood independent of mean BP or BP variability. Therefore, SBP-TTR from an early age might serve as a modifiable risk factor for future cardiovascular diseases in later life.

IntroductionThe effectiveness of remimazolam in suppressing oxidative stress, inflammatory reactions, and its lung-protective effects in patients undergoing thoracic surgery with one-lung ventilation (OLV) remains unestablished. This study aimed to investigate the protective effects of remimazolam against oxidative stress and inflammatory damage in such patients.MethodsThis randomized controlled trial evaluated 88 patients with lung tumors who underwent single-lung ventilation for thoracoscopic lobectomy under general anesthesia. Patients were randomly divided into an experimental group (R group) and a control group (Con group), with 44 patients in each group. The R group received an intravenous injection of 0.2 mg/kg of remimazolam during anesthesia induction. During anesthesia maintenance, a continuous intravenous infusion of remimazolam at a rate of 0.2 mg/kg/h was administered. The Con group received routine anesthesia. Preoperative and postoperative levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6 were detected. Changes in blood pressure and heart rate were recorded at four time points: upon entering the operating room (T1), immediately after tracheal intubation (T2), immediately after incision (T3), and immediately after surgery completion (T4). The postoperative awakening time, post-anesthesia care unit (PACU) stay time, and frequency of adverse reactions were also recorded.ResultsPostoperatively, the R group exhibited significantly higher levels of SOD and GSH-Px, and significantly lower levels of TNF-α and IL-6 compared to the Con group (P < 0.01). At T2, the blood pressure and heart rate in R group were significantly higher than those in Con group (P < 0.01), whereas no differences were found between the two groups at other time points. There were no significant differences between the two groups in postoperative awakening time, PACU stay time, or incidence of adverse reactions.DiscussionLow-dose remimazolam (0.2 mg/kg) can provide protective effects against oxidative stress and inflammatory injuries in patients undergoing OLV, without affecting awakening time or PACU time.

Childhood blood pressure (BP) is associated with increased arterial stiffness later in life. This study aimed to investigate the contributions of BP across different life stages to midlife arterial stiffness and the mediating role of metabolic factors. Using data from the Hanzhong Adolescent Hypertension Study, 1448 participants aged 6-18 years at baseline were prospectively followed for 30 years into adulthood. We used linear regression models to examine the associations between BP at different life stages and brachial-ankle pulse wave velocity (baPWV). In addition, parallel multiple mediation analyses were conducted to evaluate the mediating roles of blood glucose and lipid metabolism in these associations. Significant associations between BP and adult baPWV were observed across childhood, adulthood, and cumulative long-term BP burden, with BP in adulthood showing the strongest association. Additionally, the triglyceride-glucose index was identified as a mediator in the relationship between adult BP and midlife baPWV, with the mediation effects more pronounced among males. Our findings suggest that the detrimental impact of elevated BP on arterial stiffness begins early in life and intensifies over the lifespan, particularly during adulthood. Furthermore, the association between adult BP and arterial stiffness appears to be partially mediated by insulin resistance.

Background Previous studies have shown that elevated remnant cholesterol (RC) was associated with stroke risk. There is insufficient evidence on the relationship between 2‐year changes in RC and stroke risk in the general population. Our aim was to explore the relationship between 2‐year changes in RC and the risks of stroke and its subtypes in the general population. Methods The study included 62 443 individuals who were free of stroke from the Kailuan Study. Two‐year changes in RC was defined as the difference between the RC in 2008 and that in 2006. Multivariable‐adjusted Cox proportion models were used to examine the associations between 2‐year changes in RC with the risks of stroke and its subtypes. Results During a median follow‐up period of 10.30 years, 3780 (6.38%) stroke events occurred. The changes in RC were positively associated with the risk of stroke, after adjustment for multiple potential confounders. The hazard ratio (HR) for the Q4 group versus the Q1 group was 1.14 (95%, CI, 1.02–1.28) for stroke, and 1.18 (95% CI, 1.04–1.32) for ischemic stroke. The risks of stroke were higher in the RC increased group than the RC nonincreased group. The HR was 1.12 (95% CI, 1.04–1.20) for stroke, and 1.15 (95% CI, 1.07–1.24) for ischemic stroke. Conclusions Substantial changes in RC are associated with increased risks of stroke in the general population. Monitoring long‐term changes in RC may assist with the early identification of individuals at high risk of stroke.

Triglyceride-glucose (TyG) index was regarded as a cost-efficient and reliable clinical surrogate marker for insulin resistance (IR), which was significantly correlated with cardiovascular disease (CVD). However, the TyG index and incident CVD in non-diabetic hypertension patients remains uncertain. The aim of study was to explore the impact of TyG index level and variability on risk of CVD among non-diabetic hypertension patients. A total of 9313 hypertensive patients without diabetes aged 30–70 years in Jiangsu Province who participated in the baseline survey from January 2010 to December 2010 and were followed up to May 2020 were included in this study. The TyG index was calculated as ln [fasting triglyceride (TG) (mg/dl) × fasting plasma glucose (FPG) (mg/dl)/2] and variation degree was calculated as the TyG index at first year follow-up (2011) minus that at baseline (2010). Cox proportional analysis regression and restricted cubic spline were used to investigate the association between TyG index level as well as variability and CVD risk. Of 9313 included participants, 5423(58.23

Abstract The E‐proteinoid 3 receptor (PTGER3), a member of the prostaglandin E2 (PGE2) subtype receptor, belongs to the G‐protein‐coupled superfamily of receptors. Animal studies have demonstrated its involvement in salt sensitivity by regulating sodium reabsorption. This study aimed to investigate the association between genetic variants of PTGER3 and salt sensitivity, longitudinal blood pressure (BP) changes, and the incidence of hypertension in Chinese adults. A chronic salt intake intervention was conducted involving 514 adults from 124 families in the 2004 Baoji Salt‐Sensitivity Study Cohort in northern China. These participants followed a 3‐day regular baseline diet, followed by a 7‐day low‐salt diet (3.0 g/d) and a 7‐day high‐salt diet (18 g/d), and were subsequently followed for 14 years. The findings revealed a significant relationship between the single nucleotide polymorphism (SNP) rs17482751 of PTGER3 and diastolic blood pressure (DBP) response to high salt intervention. Additionally, SNPs rs11209733, rs3765894, and rs2268062 were significantly associated with longitudinal changes in systolic blood pressure (SBP), DBP, and mean arterial pressure (MAP) during the 14‐year follow‐up period. SNP rs6424414 was significantly associated with longitudinal changes in DBP over 14 years. Finally, SNP rs17482751 showed a significant correlation with the incidence of hypertension over 14 years. These results emphasize the significant role of PTGER3 gene polymorphism in salt sensitivity, longitudinal BP changes, and the development of hypertension in the Chinese population.