Circulating exosomal miR-20b-5p and miR-1273g-3p were potential biomarkers for diagnosis and prognosis of acute coronary syndrome

Introduction

Acute coronary syndrome (ACS) is a fatal clinical condition caused by acute myocardial ischemia, primarily resulting from coronary plaque instability and thrombosis (1). Early identification and diagnosis of ACS are critical for timely intervention, which can prevent severe disability and reduce mortality. Despite the widespread adoption of percutaneous coronary intervention (PCI), which has substantially decreased ACS-related deaths, the occurrence of major adverse cardiovascular events (MACEs) after PCI continues to threaten patient outcomes and quality of life (2). The current diagnosis of ACS is based on clinical symptoms, electrocardiogram ST-segment changes, and elevated myocardial necrosis markers. Despite being a cornerstone biomarker, cardiac troponin (cTn) has limited early diagnostic value due to its delayed release [typically ≥4 hours post-acute myocardial infarction (AMI)] and non-specific elevation in other myocardial injury conditions (3). Therefore, identifying effective biomarkers associated with the progression and prognosis of ACS remains crucial for effective ACS management.

Exosomes are nanosized extracellular vesicles, generally smaller than 150 nm, secreted by many cell types under physiological and pathological conditions (4). These vesicles possess a lipid bilayer structure and carry a diverse array of bioactive molecules, including proteins, lipids, DNA, and microRNAs (miRNAs). Exosomes are now recognized as key mediators of intercellular communication (5). Accumulating evidence indicates that exosomal miRNAs participate in multiple cardiovascular processes, influencing both physiology and pathology (6,7). For example, circulating exosomal miR-19b-3p is significantly elevated in patients with heart failure (HF) and shows strong prognostic potential (8). Similarly, cardiac-specific miR-1 and miR-133 have been detected in exosomes derived from the serum of ACS patients (9). Furthermore, miR-208a is markedly upregulated in both serum and exosomes of ACS patients, with exosomal miR-208a demonstrating superior diagnostic sensitivity compared with serum levels alone (10). Circulating miRNAs exhibit remarkable stability owing to their enrichment within exosomes, which protect them from degradation by a lipid bilayer (11). Serum extracellular vesicle miRNAs represent promising emerging biomarkers that could aid in the early diagnosis and prognostic stratification of AMI patients. In a previous study, our group identified a distinct plasma miRNA profile in ACS patients, in which miR-1273g-3p and miR-20b-5p were upregulated (12). However, the expression of exosomal miR-1273g-3p and miR-20b-5p in ACS patients remains unknown.

In the present study, we examined the exosomal miR-20b-5p and miR-1273g-3p levels in patients with ACS. The objective was to determine whether plasma-derived exosomal miR-20b-5p and miR-1273g-3p could serve as potential diagnostic and prognostic biomarkers for ACS. We present this article in accordance with the STARD reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-368/rc).

Methods

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of Meizhou People’s Hospital (No. 2025-C-146). All participants signed informed consent for research participation.

Study subjects

This retrospective study randomly included patients who were diagnosed with ACS and underwent successful PCI with drug-eluting stent (DES) implantation between October 2020 and November 2023 in the Department of Cardiology, Meizhou People’s Hospital. Blood samples were obtained on the day of hospital admission, before patients underwent PCI. The diagnosis of ACS followed the 2020 European Society of Cardiology (ESC) Guidelines for the management of ACS (13). The control group comprised patients with normal coronary arteries (NCA) as verified by coronary computed tomography angiography (CTA), such as patients diagnosed with myocardial bridging and those experiencing unexplained chest pain. Patients with HF, cardiomyopathy, congenital heart disease, severe liver or kidney dysfunction, malignancies, infections, autoimmune diseases, or psychiatric disorders were excluded.

Clinical information collection and follow-up

Baseline clinical information of the enrolled subjects was extracted from the hospital’s Electronic Medical Record System (DHC Mediway Technology, Beijing, China). Laboratory parameters, including total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), left ventricular ejection fraction (LVEF) and cardiac troponin I (cTnI) measured before PCI, were collected for analysis.

All ACS patients underwent a minimum follow-up period of 1 year after PCI. The follow-up data on MACEs were collected via the hospital’s electronic medical record system or telephone interviews. MACEs, defined as recurrent angina, HF, recurrent myocardial infarction (MI), revascularization, or sudden cardiac death, were recorded.

Exosomes isolation and characterization

Exosomes were isolated from plasma following a previously described protocol (14). Briefly, 400 µL of plasma was first centrifuged at 2,000 g for 10 min, followed by an additional spin at 10,000 g for 30 min. The resulting supernatant was diluted with an equal volume of pre-chilled phosphate-buffered saline (PBS) and filtered through a 0.22-µm membrane. Ultracentrifugation was subsequently performed twice at 120,000 g for 30 min using a CP100NX ultracentrifuge (Himac, Tokyo, Japan). The exosome-depleted supernatant (EDS) was discarded, and the pellet was resuspended in 100 µL PBS.

Exosomal morphology was visualized by transmission electron microscopy (TEM) (JEM-1400, JEOL, Akishima, Japan). Particle size and concentration were determined by nanoparticle tracking analysis (NTA) (Malvern Panalytical, Worcestershire, UK). Western blotting was used to detect exosomal protein markers with specific primary antibody against CD9, CD63, and TSG101 (1:1,000, Cell Signaling Technology, Boston, USA).

RNA isolation and reverse transcription-quantitative polymerase chain reaction (RT-qPCR)

Small RNA was isolated using the SteadyPure Small RNA Extraction Kit (Accurate Biology, Changsha, China). Complementary DNA (cDNA) was generated by Mir-X miRNA First-Strand Synthesis Kit (Takara, Dalian, China). The expression of miRNAs was determined using the TB Green^® Premix Ex Taq^TM II (Takara, Dalian, China). Relative expression of miRNAs was normalized to U6 using the 2^−ΔΔCt method. Primer sequences were as follows: miR-20b-5p, 5’-CAAAGUGCUCAUAGUGCAGGUAG-3’; miR-1273g-3p, 5’-ACCACUGCACUCCAGCCUGAG-3’; U6 forward, 5’-GGAACGATACAGAGAAGATTAGC-3’; and U6 reverse, 5’-TGGAACGCTTCACGAATTTGCG-3’.

Statistical analysis

All statistical analyses were performed using SPSS version 20.0 (IBM Corp., Armonk, NY, USA). Continuous variables were presented as mean ± standard deviation (SD), while categorical variables were summarized as frequencies and percentages. Between-group comparisons of continuous data were assessed with the Student’s t-test, and categorical data were analyzed using the Chi-squares (χ²) test or Fisher’s exact test when applicable. Receiver operating characteristic (ROC) curve analysis was conducted to determine the diagnostic value of exosomal miRNAs in ACS. The prognostic significance of exosomal miRNA expression for MACEs following PCI was evaluated using multivariable Cox proportional hazards regression. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated adjusted for variables such as age, gender, diabetes mellitus, hypertension and dyslipidemia. A two-sided P value <0.05 was considered statistically significant.

Results

Baseline characteristics of the study participants

A total of 138 patients with ACS were enrolled, with a mean age of 65.54±10.60 years. The control cohort comprised 129 NCA individuals, with a mean age of 61.28±8.50 years. Baseline clinical characteristics are summarized in Table 1. Significant differences were observed in age, LVEF, cTnI, and Gensini score between ACS patients and controls, while no significant differences were found for other baseline variables.

Characterization of plasma exosomes

Plasma exosomes were analyzed by TEM, NTA and western blotting. TEM revealed vesicles with a typical cup-shaped morphology and diameters ranging from 40 to 150 nm (Figure 1A). NTA analysis showed an average particle size of approximately 142 nm (Figure 1B). Western blotting verified the expression of exosomal markers CD9, TSG101, and CD63, which were absent in the EDS (Figure 1C).

Figure 1 Characterization of plasma-derived exosomes. (A) Exosome morphology visualized by TEM. Representative exosomes are indicated by arrows. (B) Particle size distribution of exosomes via NTA. (C) Detection of exosomal markers by western blot. EDS, exosome-depleted supernatant; NTA, nanoparticle tracking analysis; TEM, transmission electron microscopy.

Expression of exosomal miR-20b-5p and miR-1273g-3p in ACS patients

Exosomal miR-20b-5p and miR-1273g-3p expression levels were quantified by RT-qPCR. Both miRNAs were upregulated in ACS patients compared with NCA controls (Figure 2A,2B). Since the ACS cohort included patients with UA and AMI, subgroup analysis was performed. No significant differences in expression levels of either miRNA were detected between UA and AMI patients (Figure 2C,2D). Similarly, comparison between STEMI and NSTEMI groups revealed no statistically significant variation in miR-20b-5p or miR-1273g-3p expression (Figure 2E,2F).

Figure 2 Exosomal miR-20b-5p and miR-1273g-3p expression in patients with ACS. The expression of exosomal miR-20b-5p (A) and miR-1273g-3p (B) in ACS patients and NCA controls was examined by RT-qPCR. The expression of exosomal miR-20b-5p (C) and miR-1273g-3p (D) in UA and AMI patients was examined by RT-qPCR. The expression of exosomal miR-20b-5p (E) and miR-1273g-3p (F) in STEMI and NSTEMI patients was examined by RT-qPCR. ACS, acute coronary syndrome; AMI, acute myocardial infarction; NCA, normal coronary artery; NSTEMI, non-ST-elevation myocardial infarction; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; STEMI, ST-elevation myocardial infarction; UA, unstable angina.

Diagnostic value of exosomal miR-20b-5p and miR-1273g-3p in ACS

ROC curve analysis was applied to evaluate the diagnostic performance of these exosomal miRNAs. The area under the curve (AUC) for miR-20b-5p was 0.705 (95% CI: 0.639–0.771) when comparing ACS patients with NCA controls. For miR-1273g-3p, the AUC was 0.720 (95% CI: 0.657–0.783). When combined with cTnI, diagnostic accuracy improved substantially, with AUC values rising to 0.818 (95% CI: 0.764–0.871) for miR-20b-5p and 0.794 (95% CI: 0.737–0.850) for miR-1273g-3p (Figure 3 and Table 2).

Figure 3 Diagnostic performance of exosomal miR-20b-5p and miR-1273g-3p in ACS. (A) ROC curves of exosomal miR-20b-5p, cTnI, and combined cTnI + miR-20b-5p for distinguishing ACS patients from NCA controls; (B) ROC curves of exosomal miR-1273g-3p, cTnI, and combined cTnI + miR-1273g-3p for distinguishing ACS patients from NCA controls. ACS, acute coronary syndrome; AUC, area under the curve; cTnI, cardiac troponin I; NCA, normal coronary artery; ROC, receiver operating characteristic.

Correlation between the exosomal miRNAs and MACE-free survival post-PCI

To evaluate the prognostic significance of exosomal miR-20b-5p and miR-1273g-3p, ACS patients were followed for 1 year after PCI. During follow-up, MACEs occurred in 18.54% (22/138) of patients. Expression of miR-20b-5p was higher in patients who experienced MACEs compared with those without events (P<0.001), whereas miR-1273g-3p expression showed no significant difference (P=0.30) (Figure 4A,4B).

Figure 4 Prognostic value of exosomal miR-20b-5p and miR-1273g-3p in ACS patients after PCI treatment. (A,B) Comparison of exosomal miR-20b-5p and miR-1273g-3p expression between the non-MACE and MACE groups. (C,D) Kaplan-Meier curves of exosomal miR-20b-3p and miR-1273g-3p for MACE-free survival in ACS patients after PCI treatment. ACS, acute coronary syndrome; MACE, major adverse cardiovascular event; PCI, percutaneous coronary intervention.

ACS patients were categorized into two groups based on exosomal miR-20b-5p expression levels: a high miR-20b-5p expression group (≥1.24, n=62) and a low miR-20b-5p expression group (<1.24, n=62). Similarly, they were also divided into a high miR-1273g-3p expression group (≥1.54, n=62) and a low miR-1273g-3p expression group (<1.54, n=62) according to exosomal miR-1273g-3p expression levels. Patients with high miR-20b-5p had a significantly greater incidence of MACEs than those with low levels (P=0.01, Table 3). However, no significant differences were observed in the incidence of refractory angina, recurrent MI, unplanned PCI, stent thrombosis, or death between the two groups. Other baseline clinical characteristics were also comparable (all P>0.05, Table 3). Kaplan-Meier analysis confirmed that high miR-20b-5p expression was associated with reduced MACE-free survival (P=0.01, Figure 4C).

In contrast, exosomal miR-1273g-3p expression showed no significant association with either MACE incidence (P=0.34, Table 4) or MACE-free survival (P=0.37, Figure 4D).

Binary Cox regression analysis was performed to identify predictors of 1-year MACEs in ACS patients after PCI. The results indicated that age [hazard ratio (HR) =2.151, 95% CI: 1.058–4.375, P=0.03], and high miR-20b-5p expression (HR =2.893, 95% CI: 1.132–7.393, P=0.02) were significantly associated with MACE risk (Table 5). Multivariable Cox regression further demonstrated that elevated miR-20b-5p remained independently linked to 1-year MACEs after adjustment for age, sex, and cardiovascular risk factors (HR =3.107, 95% CI: 1.157–8.340, P=0.02; Figure 5).

Figure 5 Multivariable Cox regression model for predicting the 1-year MACEs in ACS patients after PCI. ACS, acute coronary syndrome; CI, confidence interval; HR, hazard ratio; MACE, major adverse cardiovascular event; PCI, percutaneous coronary intervention.

Discussion

Early diagnosis, appropriate prevention, and timely treatment are critical for reducing the morbidity and mortality of ACS. Our study demonstrated that plasma-derived exosomal miR-20b-5p and miR-1273g-3p were markedly upregulated in ACS patients, indicating their potential as circulating diagnostic indicators. Moreover, elevated exosomal miR-20b-5p was significantly associated with reduced 1-year MACE-free survival after PCI.

The clinical features of the enrolled cohort were consistent with previous reports, with a mean age of over 60 years and more than 60% of cases being male (15). The ACS cohort included patients with UA and AMI, all of whom underwent successful PCI with DES implantation and completed at least 1 year of regular follow-up in our hospital. Controls consisted of individuals presenting with angina-like chest pain or discomfort but with angiographically confirmed NCA. ACS patients and NCA controls were comparable in terms of age, sex, and history of hypertension and diabetes, supporting the representativeness of the study population.

In recent years, exosome-carried miRNAs have attracted increasing attention as biomarkers in cardiovascular diseases. Distinct exosomal miRNA expression profiles have been reported in patients with cardiovascular conditions, along with their associations with prognosis. For example, exosomal miR-122-5p in AMI patients was positively correlated with Gensini scores and associated with a lower incidence of MACEs (16). Li et al. reported that serum exosomal miRNA-146a was increased in ACS patients compared with the NCA control group, and exhibited a good diagnostic performance for ACS (17). Hou et al. (18) discovered that exosomal mascRNA [a transfer RNA (tRNA)-like small non-coding RNA] levels were elevated in the plasma of ACS patients and demonstrated significant diagnostic value for ACS. In our study, exosomal miR-20b-5p was elevated in ACS patients and demonstrated diagnostic potential. Although the diagnostic performance of exosomal miR-20b-5p is not as good as miRNA-146a or mascRNA, we assume the differences may be attributed to some factors like sample size, inclusion criteria. Notably, when combined miR-20b-5p with cTnI, diagnostic accuracy improved, achieving an AUC of 0.818. Interestingly, a recent study reported that higher baseline levels of circulating miR-20b-5p were associated with improved in-hospital and 90-day survival in patients with cardiogenic shock, whereas our findings indicated that elevated exosomal miR-20b-5p was positively correlated with MACEs in ACS patients. Other microRNAs, such as miR-133, miR-208b, and miR-499, have also demonstrated strong diagnostic performance in ACS, in some cases surpassing troponins for early detection of the condition. These miRNAs are released directly from apoptotic cardiomyocytes due to their close association with myosin, making them sensitive markers of myocardial injury (19,20). Moreover, certain miRNAs exhibit differential expression between STEMI and NSTEMI patients. For instance, circulating miR-124 and miR-133a/b were elevated in patients with an occluded coronary artery compared with those with a patent vessel (19,20). In contrast, our analysis revealed no significant variation in exosomal miR-20b-5p or miR-1273g-3p expression between these subgroups. Further large-scale, prospective clinical investigations are warranted to elucidate the precise role and underlying mechanisms of miR-20b-5p in the pathogenesis of ACS.

Previous studies have demonstrated that exosomes secreted by monocytes, vascular smooth muscle cells (VSMCs), and endothelial cells influence the function of target cells and contribute to the progression of atherosclerosis (AS) (21-23). During vascular injury, exosomal miR-150 derived from VSMCs was shown to regulate endothelial cell migration by targeting chemokine (C-X-C motif) ligand 12 (CXCL12), thereby impairing re-endothelialization after injury (24). Endothelial cells can release exosomal miR-204-5p, which is delivered to SMCs and suppresses vascular calcification by modulating RUNX2 expression (24). In addition, inhibition of miR-20b-5p has been reported to attenuate reactive oxygen species (ROS) generation, reduce SA-β-gal activity, and decrease the expression of senescence-related proteins p16 and p21 in human umbilical vein endothelial cells, underscoring its role in endothelial cell senescence (25). The cellular source of exosomal miR-20b-5p was not identified in this study, although inflammatory endothelial cells are likely contributors. Future investigations should focus on elucidating the mechanistic contributions of exosomal miR-20b-5p and miR-1273g-3p to ACS pathogenesis at the molecular and cellular levels, particularly in the context of plaque rupture and thrombosis. It would be of interest to examine whether these miRNAs regulate key processes such as endothelial activation, inflammation, and ferroptosis through silencing of candidate target genes involved in inflammatory, apoptotic, or thrombotic pathways. Furthermore, evaluating the spatiotemporal release of these miRNAs from specific cell types within unstable plaques may provide critical insights into their role as intercellular mediators driving ACS progression.

This study has some limitations. First, as a single-center retrospective study, the limited sample size may affect the reliability of the conclusions. Second, the dynamic changes in exosomal miRNA levels after the onset of ACS were not assessed, which may be important for determining the optimal timing of miRNA detection and improving diagnostic and prognostic accuracy. Future studies should employ large-scale, prospective cohorts and evaluate exosomal miRNA expression at critical time points following ACS onset to define the optimal diagnostic window for these biomarkers.

Conclusions

In summary, the levels of exosomal miR-20b-5p and miR-1273g-3p were markedly elevated in the plasma of patients with ACS compared to NCA controls, indicating significant diagnostic potential for ACS. Furthermore, exosomal miR-20b-5p was associated with the incidence of MACEs, thereby offering prognostic value for ACS.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STARD reporting checklist. Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-368/rc

Data Sharing Statement: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-368/dss

Peer Review File: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-368/prf

Funding: This study was supported by the Guangdong Basic and Applied Basic Research Foundation (No. 2024A1515010809); Scientific Research and Cultivation Project of Meizhou People’s Hospital (No. PY-C2023009); State Key Laboratory of Neurology and Oncology Drug Development (No. SKLSIM-F-202412).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-368/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of Meizhou People’s Hospital (No. 2025-C-146). All participants signed informed consent for research participation.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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