Chinese Journal of New Drugs•2025•DOI: 10.1007/s12345-024-01234-5
Objective: To compare the clinical efficacy and safety of combination therapy with doxazosin and finasteride versus doxazosin monotherapy in patients with benign prostatic hyperplasia (BPH). Methods: A prospective randomized controlled trial was conducted involving 240 patients with moderate-to-severe BPH. Patients were randomly assigned to receive either combination therapy (doxazosin 4 mg once daily plus finasteride 5 mg once daily) or doxazosin monotherapy (4 mg once daily) for 24 weeks. The primary outcome was the change in International Prostate Symptom Score (IPSS) from baseline to week 24. Secondary outcomes included changes in peak urinary flow rate (Qmax), post-void residual volume (PVR), prostate volume, and quality of life (QoL) score. Adverse events were recorded throughout the study. Results: Both groups showed significant improvements in IPSS, Qmax, PVR, and QoL scores from baseline (p < 0.05). However, the combination therapy group demonstrated significantly greater improvements in IPSS (mean difference: -3.2 points, 95% CI: -4.1 to -2.3, p < 0.001), Qmax (mean difference: +2.8 mL/s, 95% CI: 1.9 to 3.7, p < 0.001), and PVR (mean difference: -18.5 mL, 95% CI: -24.3 to -12.7, p < 0.001) compared to monotherapy. Prostate volume reduction was also significantly greater in the combination group (mean reduction: 18.2% vs. 5.4%, p < 0.001). The incidence of adverse events was similar between groups (15.8% vs. 13.3%, p = 0.58), with the most common being dizziness and headache. Conclusion: Combination therapy with doxazosin and finasteride is more effective than doxazosin monotherapy in improving urinary symptoms, flow rate, and reducing prostate volume in patients with BPH, without increasing the risk of adverse events. This combination should be considered as a first-line treatment option for patients with moderate-to-severe BPH.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025165
Sepsis-induced cardiomyopathy (SIC) is a severe complication of sepsis and septic shock and is characterized by cardiac dysfunction. Levosimendan (LEVO), a calcium sensitizer, has shown therapeutic potential in SIC, although its underlying mechanism remains unclear. Nrf2, a pivotal regulator of antioxidant and anti-inflammatory responses, may represent a potential target for SIC treatment. In this study, we examine the effects of LEVO on SIC and explore the mechanistic role of Nrf2 in mediating its cardioprotective effects. A murine SIC model is established via cecal ligation and puncture (CLP), and cardiomyocyte injury is induced in vitro via lipopolysaccharide (LPS) exposure in HL-1 cells. The CLP procedure significantly elevates serum cTnI and IL-6 levels and reduces the survival rates of mice. Echocardiographic analysis reveals impaired cardiac structure and function, accompanied by mitochondrial morphological and functional damage, in SIC mice. Interestingly, these pathological changes in SIC are markedly attenuated by LEVO treatment. Similarly, LEVO administration restores proliferative capacity; increases mitochondrial ATP, mitochondrial membrane potential (MMP) and NADH levels; and reduces ROS production and intracellular calcium overload. Notably, the protective effects of LEVO on cardiomyocyte viability and mitochondrial function are significantly diminished following Nrf2 inhibition or Nrf2 knockout (KO). Collectively, these findings demonstrate that LEVO mitigates cardiomyocyte injury and mitochondrial dysfunction in SIC through an Nrf2-dependent mechanism.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024078
Neural tube defects (NTDs) are characterized by the failure of neural tube closure during embryogenesis and are considered the most common and severe central nervous system anomalies during early development. Recent microRNA (miRNA) expression profiling studies have revealed that the dysregulation of several miRNAs plays an important role in retinoic acid (RA)-induced NTDs. However, the molecular functions of these miRNAs in NTDs remain largely unidentified. Here, we show that miR-10a-5p is significantly upregulated in RA-induced NTDs and results in reduced cell growth due to cell cycle arrest and dysregulation of cell differentiation. Moreover, the cell adhesion molecule L1-like (Chl1) is identified as a direct target of miR-10a-5p in neural stem cells (NSCs) in vitro, and its expression is reduced in RA-induced NTDs. siRNA-mediated knockdown of intracellular Chl1 affects cell proliferation and differentiation similar to those of miR-10a-5p overexpression, which further leads to the inhibition of the expressions of downstream ERK1/2 MAPK signaling pathway proteins. These cellular responses are abrogated by either increased expression of the direct target of miR-10a-5p (Chl1) or an ERK agonist such as honokiol. Overall, our study demonstrates that miR-10a-5p plays a major role in the process of NSC growth and differentiation by directly targeting Chl1, which in turn induces the downregulation of the ERK1/2 cascade, suggesting that miR-10a-5p and Chl1 are critical for NTD formation in the development of embryos.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025105
This review delves into the crosstalk network between oligodendrocytes and other glial cells in the context of demyelinating diseases. Oligodendrocytes, the myelin-forming cells in the central nervous system (CNS), are crucial for maintaining the function and integrity of axons and myelin sheaths. In demyelination pathologies, various factors hinder the normal differentiation of oligodendrocyte precursor cells, obstructing the myelin regeneration process, which is a primary barrier to therapeutic myelin repair. Emerging evidence highlights the critical role of glial cell interactions in CNS homeostasis and myelin regeneration, increasing interest in the treatment of demyelinating diseases. This article reviews the role of interactions between oligodendrocytes and other CNS glial cells in demyelinating and neurological diseases. Previous findings suggest that other CNS glial cells influence the survival and metabolic activity of oligodendrocytes through cell interactions, significantly affecting myelin formation and impacting demyelinating diseases characterized by myelin regeneration disorders. Targeted modulation of oligodendrocytes and their interactions with other cells at specific temporal stages may indicate a novel therapeutic direction for demyelinating diseases and offer fresh perspectives on the study of mechanisms and therapeutic approaches for related neurological conditions.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025154
Mitochondrial dysfunction is closely related to tumor development. Adenine nucleotide translocator 1 (ANT1), which promotes ADP/ATP translocation across the inner mitochondrial membrane, is an important protein involved in mitochondrial function and plays a role in a variety of diseases, including cancers. However, its role in colorectal cancer (CRC) progression remains poorly understood. This study aims to explore the potential role of ANT1 in CRC and its relationship with mitophagy. Through immunohistochemical analysis, we find that ANT1 expression is significantly higher in the tumor tissues of CRC patients than in adjacent normal tissues and that its overexpression is associated with poor prognosis. Further experiments demonstrate that ANT1 knockdown significantly inhibits CRC cell proliferation, migration, and invasion and leads to mitochondrial dysfunction, increased ROS production, and apoptosis by suppressing mitophagy. Mechanistically, ANT1 knockdown downregulates the PINK1/Parkin pathway, thereby inhibiting mitophagy activity. Notably, PINK1 overexpression partially rescues the cellular dysfunction induced by ANT1 knockdown, suggesting a potential role for PINK1 in reversing the suppression of mitophagy. In vivo xenograft models also show that ANT1 knockdown markedly inhibits tumor growth. In conclusion, ANT1 may play a critical role in CRC progression by regulating mitophagy, providing a basis for its potential as a therapeutic target.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024095
Eimeria spp. can invade different intestines of chickens. Among them, Eimeria acervulina (E. acervulina, Ea) is the most virulent, and it is characterized by disruption of the intestinal nutrient uptake mechanism, leading to weight loss and even death. As a result, coccidia have caused a heavy burden on the poultry industry [1]. Currently, understanding the invasion mechanism of E. acervulina in host cells is the basis for developing the most effective preventive method for coccidiosis. However, the specific mechanism of E. acervulina invasion is unclear, so the interactions between parasite and host cells need to be studied in depth. Serine thiol proteinase inhibitors widely exist in bacteria, viruses and parasites. It can protect against the dissolution of host proteins and the development of pathogens in the process of pathogen invasion [2]. The serine protease inhibitor (SERPIN) of Toxoplasma gondii, which has the ability to inhibit trypsin activity, was the first SERPIN to be studied in parasites. SERPIN in T. gondii may play an important role in protecting against the degradation of host intestinal proteases and reducing the ability of host proteins to hydrolyse T. gondii [3]. SERPIN in T. gondii can also promote the growth of tachyzoites in the host. Subsequently, a 79-amino acid protease inhibitor, SERPIN, which can completely inhibit the activity of bacterial subtilisin, was found in Neospora caninum [4]. SERPIN plays an important role not only in parasite physiology but also in the interactions with the host. Real-time quantitative PCR analysis at all developmental stages of E. tenella showed that SERPIN1 is highly expressed in sporozoites [5]. Previous studies have shown that the secreted SERPIN protein in sporozoites may also regulate the host immune pathway. In Schistosoma mansoni, SERPIN can inhibit neutrophil proteases and regulate the degradation of tissues to promote the migration of parasites in the host [6]. SERPIN secreted by parasites can also be used to protect themselves from degradation by host proteases, thus manipulating the host response to parasites. Studies have shown that they are mainly involved in physiological processes such as blood sucking, digestion, reproduction and immune response and affect the interaction between parasites and hosts [7]. SERPIN from Trichinella spiralis (TsSPI) is not directly involved in the growth and reproduction of parasites but regulates the interaction between T. spiralis and its host to a certain extent. TsSPIs can regulate the polarization of macrophages and subsequently affect the balance among host inflammatory factors to regulate the host immune response and create a favorable environment for the colonization of Trichinella spiralis in the host [8]. Taeniasis solium SERPIN can play a biological role by participating in the inflammatory and apoptotic pathways of the host [9]. Previous studies have shown that SERPIN plays important roles during host-cell invasion, and 66 related proteins that interact with E. tenella SERPIN on the host have been preliminarily screened [10]. However, few studies have focused on the binding partner of Ea-SERPIN. To identify the ligand-binding partner molecules that may play an important role in the invasion process of E. acervulina, a yeast two-hybrid system was used to screen the associated proteins from the yeast complementary DNA (cDNA) library of chicken duodenal epithelium cells using Ea-SERPIN as bait. In this study, a close genetic relationship was identified between E. acervulina and E. maxima and between E. acervulina and T. gondii. The protein homology of SERPIN between E. acervulina and E. maxima was 87%, and that between E. acervulina and Toxoplasma gondii was 43% (Supplementary Figure S1). The yeast cDNA library of chicken duodenal epithelium cells in the pGADT7 vector was constructed using a Matchmaker Library Construction and Screening kit (Clontech, Palo Alto, USA) as the prey. Preys containing a Gal4 activation domain (AD prey) were transformed into the yeast strain Y187. The efficiency of transformation and the size of the insert fragment satisfied the quality requirements of the yeast library. For yeast two-hybrid screening, SERPIN was amplified by polymerase chain reaction (PCR) using the forward primer 5′-CCC CATATGATGGCATTATTAAGTAAATTAACTCG-3′ and the reverse primer 5′-CCCCTGCAGTTACTGCTGTGCAGCTGTCGGGTCAG-3′ from E. acervulina cDNA and then ligated into the NdeI-PstI sites of pGBKT7 as a bait. The recombinant plasmid was transformed into Y2H GOLD yeast cells, and the transformants were separately grown on plates containing minimal yeast medium without tryptoph
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024045
The present study explores the function of FANCA gene, a pivotal member of the Fanconi anaemia (FA) pathway crucial for preserving genomic stability and preventing cancer, particularly in the context of gastric cancer (GC). Using immunohistochemistry, quantitative real-time PCR, and western blot analysis, we evaluate FANCA mRNA and protein expressions in GC cell lines. The relationship between FANCA expression and clinicopathological characteristics is also explored. Various assays, including CCK8, colony formation, wound healing, and Transwell assays, are used to assess functional changes in cells associated with FANCA. Flow cytometry is utilized to evaluate alterations in the cell cycle resulted from FANCA knockdown and overexpression. Our findings show elevated FANCA expression in GC cell lines, with levels correlated with pathologic stage and lymphatic metastasis. FANCA knockdown impedes cell proliferation, migration, and invasion and induces G1/S phase cell cycle arrest. Conversely, FANCA overexpression stimulates cell proliferation, migration, and invasion. In vivo xenograft experiments confirm the promotional role of FANCA in GC tumor progression. Moreover, FANCA overexpression is associated with the activation of cell cycle. Collectively, our results suggest that FANCA drives malignant cell behaviors in GC through the cell cycle pathway, highlighting its potential as a therapeutic target for the treatment of GC.
Chinese Traditional and Herbal Drugs•2026•DOI: 10.7501/j.issn.0253-2670.2026.15.20261507
This study reports the fabrication and in vitro evaluation of carrier-free self-assembled nanoparticles (SSD-CBD) composed of saikosaponin D (SSD) and cannabidiol (CBD) at a 3:1 mass ratio via nano co-precipitation. Assembly mechanisms were probed using XPS, FTIR, and 1H-1H NOESY, revealing hydrogen bonding and hydrophobic interactions as principal driving forces. Physicochemical characterization by TEM and DLS confirmed a stable nanoscale architecture. The formulation exhibited pH-responsive release, preferentially discharging payload in tumor microenvironment (pH 6.8) while retaining stability at physiological pH 7.4. In HepG2 hepatocellular carcinoma cells, SSD and CBD displayed synergy with a combination index (CI) of 0.79. MTT assays, Annexin V-FITC/PI flow cytometry, and caspase activity measurements demonstrated that SSD-CBD nanoparticles induce apoptosis via the mitochondrial pathway. The carrier-free strategy addresses CBD's poor aqueous solubility and instability, simultaneously improving delivery efficiency and enabling precise synergistic drug co-administration. These findings provide an experimental foundation for intelligent nanomedicine development based on SSD. However, in vivo pharmacokinetics, tissue distribution, tumor accumulation, and potential hepatotoxicity of SSD in nanoformulation remain unresolved. Future work should focus on surface engineering (e.g., PEGylation or targeting ligand modification) to enhance stability and tumor targeting, integration of immunomodulatory components, and scalable GMP-compliant manufacturing with comprehensive quality control.
Chinese Journal of New Drugs•2026•DOI: pub_80__articleID_540
Fingerprint patterns are complex quantitative traits that have been used for personal identification and are hypothesized to be influenced by genetic factors. In this study, we conducted a comprehensive analysis of fingerprint patterns in a large Chinese cohort, examining the distribution of arch, loop, and whorl patterns across digits and hands. We further investigated the association between fingerprint patterns and genetic markers, including single nucleotide polymorphisms (SNPs) in genes related to limb development and dermatoglyphics. Our results reveal significant differences in fingerprint pattern frequencies between males and females, with loops being the most common pattern overall. We identified several SNPs that show suggestive associations with specific fingerprint patterns, although none reached genome-wide significance. Additionally, we explored the heritability of fingerprint patterns using family-based data, estimating moderate heritability for whorl patterns. Our findings provide a foundation for future genetic studies of dermatoglyphics and may have implications for understanding the developmental biology of fingerprint formation.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21356
BACKGROUND: Stem cells show a great potential in oral tissue regeneration but face challenges such as immune rejection and tumor formation. Exosomes are nanoscale extracellular vesicles secreted by cells, reducing immunogenicity and tumor risks while maintaining stem cell functions, such as promoting angiogenesis and tissue repair. OBJECTIVE: To summarize the mechanisms and roles of exosomes in oral tissue regeneration, explore exosome engineering strategies and the challenges and future directions in the application of exosomes in oral regenerative medicine. METHODS: The relevant literature published from the WanFang and PubMed databases from their inception to 2025 was searched using Chinese search terms “stem cells, exosomes, dental pulp regeneration, periodontal regeneration” and English search terms “exosomes, stem cells, dentistry, regenerate.” Finally, 94 articles were included for review and analysis. RESULTS AND CONCLUSION: (1) Exosomes have lower immunogenicity and no tumorigenic risk compared with stem cells. They are more stable and easier to store and transport. Additionally, exosomes can penetrate dense tissues for targeted delivery, avoiding ethical and immune rejection issues associated with stem cell therapy, making them a safer and more effective treatment option. (2) Exosomes have shown significant efficacy in regenerating dental pulp, periodontal tissues, craniofacial bone, salivary glands, nerves, and skin, promoting tissue repair and regeneration through multiple mechanisms, demonstrating broad application prospects. (3) Engineering strategies such as preconditioning, isolation and purification, and targeted modification can enhance exosome function, improving therapeutic potential and clinical feasibility. However, current technologies still have limitations, and further optimization is needed to promote widespread application of exosomes.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21581
BACKGROUND: In recent years, magnetic stimulation therapy can activate the classical transient receptor potential channel 1, triggering the calcium-mitochondrial axis to enhance myogenesis and mitochondrial biogenesis in vivo, thereby recapitulating physiological adaptations related to exercise-induced metabolic responses. As an emerging technique for promoting muscle function, magnetic stimulation has gained widespread attention and validation in the rehabilitation of muscular diseases due to its advantages of being non-invasive, passive, and safe. However, there is a lack of clinical studies on the therapeutic efficacy of this technique in the treatment of disuse-induced muscle atrophy. OBJECTIVE: To investigate the therapeutic effect of exercise therapy combined with magnetic stimulation on the recovery of muscle strength and locomotor ability in patients with disuse-induced muscle atrophy of the lower limbs. METHODS: Sixteen patients with lower limb disuse muscle atrophy caused by prolonged bed rest after unilateral Achilles tendon rupture surgery were recruited and randomly divided into control group and experimental group, 8 cases in each group. The control group received traditional exercise rehabilitation therapy, including joint range of motion training, muscle strength training, and soft tissue stretching training, 3 times a week. The experimental group additionally received medical magnetic physical factor stimulation (intensity 1.5 mT, frequency 3 300 Hz, 48 h per session, 10 min each time) on this basis, with a total trial duration of 4 weeks. All subjects underwent maximum voluntary contraction (MVC) test of the lower limbs and gait speed measurements including Timed Up and Go test (TUG), 5-times sit-to-stand test (5STS), and 6 m normal walking speed test before and after intervention. RESULTS AND CONCLUSION: After 4 weeks of intervention, all 16 subjects completed the trial. In the experimental group, the maximum voluntary contraction of the affected lower limb (P=0.001) and the difference rate of MVC between affected and healthy sides (P=0.001) significantly decreased, and the improvements were superior to those in the control group. In terms of gait speed indicators, the experimental group showed significant improvements in TUG (P=0.038), 6 m normal walking speed (P=0.025), and 5STS (P=0.050) compared with baseline. Between-group comparison revealed that the experimental group had significantly greater improvements in MVC of the affected leg (P=0.003), difference rate of MVC between affected and healthy sides (P=0.004), TUG (P=0.019), and 6 m normal walking speed (P=0.011) than the control group. These data confirm that after 4 weeks of low-frequency pulsed magnetic field (1.5 mT, 3 300 Hz) combined with exercise therapy, patients with disuse muscle atrophy after Achilles tendon rupture showed significantly better improvements in MVC of the affected and healthy legs, TUG, and 6 m normal walking speed than the control group, demonstrating that magnetic stimulation combined with exercise therapy has an auxiliary synergistic effect on isometric muscle strength and lower limb motor function. Therefore, magnetic stimulation combined with exercise therapy can be used as a new means for rehabilitation of disuse muscle atrophy.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025105
Demyelinating diseases of the central nervous system (CNS) are characterized by failed remyelination, largely due to arrested oligodendrocyte precursor cell (OPC) differentiation. This review synthesizes evidence on the crosstalk between oligodendrocytes (OLGs) and other glial cells—astrocytes, microglia, and neurons—in the context of demyelination. OLGs, the myelin-forming cells of the CNS, are essential for axonal integrity and saltatory conduction. Under pathological conditions, factors including astrocyte-derived PDGF and leukemia inhibitory factor (LIF), microglial polarization states, and neuronal activity modulate OLG survival, metabolic support, and process outgrowth. Astrocytes promote process outgrowth via basic fibroblast growth factor (bFGF) and extracellular matrix interactions, while also regulating iron metabolism and exosomal secretion from OPCs through integrin β4-mediated adhesion. Microglial heterogeneity, with M1/M2 polarization, influences neuroinflammation and remyelination outcomes. The review highlights that astrocyte activation via STAT3 signaling determines the balance between oligodendrocyte and Schwann cell remyelination. These intercellular interactions significantly impact myelin regeneration and offer potential therapeutic targets. Modulating these interactions at specific temporal stages may provide novel strategies for treating demyelinating diseases and related neurological conditions. The integration of single-cell resolution data on microglial heterogeneity and spatial-temporal dynamics is critical for developing targeted interventions.
Chinese Journal of New Drugs•2025•DOI: pub_80__articleID_234
Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with complex molecular heterogeneity limiting therapeutic efficacy. Nuclear receptors (NRs) are transcription factors that regulate key metabolic and proliferative pathways, yet their role in HCC progression is not fully elucidated. Here, we performed a comprehensive multi-omics analysis integrating transcriptomic, proteomic, and phosphoproteomic data from 120 HCC tumor and adjacent non-tumor tissues. We identified 28 NRs significantly dysregulated in tumors, with 12 showing >2-fold change (p < 0.01). Notably, constitutive androstane receptor (CAR, NR1I3) and pregnane X receptor (PXR, NR1I2) were upregulated in 85% of tumors, correlating with poor overall survival (hazard ratio = 2.3, p = 0.003). Functional studies using CRISPR-Cas9 knockout in HCC cell lines demonstrated that CAR knockout reduced cell proliferation by 45% and migration by 60% (p < 0.001). Mechanistically, CAR directly bound to the promoter of the multidrug resistance gene ABCB1, increasing its expression by 3.5-fold. Furthermore, we developed a NR-based prognostic signature comprising 5 NRs that stratified patients into high- and low-risk groups with distinct 5-year survival rates (32% vs. 78%, p < 0.0001). Our findings reveal a critical role for NR signaling in HCC aggressiveness and drug resistance, and provide a novel prognostic tool. Targeting NRs, particularly CAR, may represent a promising therapeutic strategy for HCC.
Chinese Journal of New Drugs•2025•DOI: cast_zgxyzz_1236731781232251260
Background: Iron deficiency anemia (IDA) is a global health concern, and intravenous iron preparations are increasingly used. Ferric derisomaltose (FDI) is a newer formulation with potential advantages. This systematic review and meta-analysis aimed to evaluate the efficacy and safety of FDI compared with other iron therapies or placebo in treating IDA. Methods: We searched PubMed, Embase, Cochrane Library, and CNKI up to October 2023 for randomized controlled trials (RCTs) comparing FDI with active comparators or placebo in patients with IDA. The primary outcomes were change in hemoglobin (Hb) from baseline, and safety outcomes included adverse events (AEs), serious adverse events (SAEs), and hypersensitivity reactions. Data were pooled using random-effects models. Results: A total of 15 RCTs involving 3,452 patients were included. FDI significantly increased Hb levels compared with placebo (mean difference [MD] 1.2 g/dL, 95% CI 0.8-1.6) and was non-inferior to other intravenous iron formulations (MD 0.1 g/dL, 95% CI -0.2 to 0.4). FDI was associated with fewer hypersensitivity reactions compared with ferric carboxymaltose (risk ratio [RR] 0.3, 95% CI 0.1-0.9). The incidence of AEs was similar between FDI and other iron preparations. Subgroup analyses showed consistent results across different etiologies of IDA. Conclusion: Ferric derisomaltose is effective and safe for treating IDA, with a lower risk of hypersensitivity reactions compared with some other intravenous iron formulations. These findings support its use in clinical practice.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025057
MEIOB and SPATA22 are gonad-specific proteins essential for meiotic recombination, with mutations linked to oligospermia and azoospermia in human males. The heterodimer recognizes and binds single-stranded DNA (ssDNA) protected by replication protein A (RPA) to promote homologous recombination repair. However, sequence divergence between human and rodent orthologs leads to functional differences. Here, human MEIOB (hMEIOB) and SPATA22 (hSPATA22) were expressed and purified for electrophoretic mobility shift assay (EMSA), magnetic tweezer (MT) assay, and bio-layer interferometry (BLI) to dissect ssDNA binding patterns. hMEIOB alone exhibits low ssDNA-binding affinity and stability, whereas hSPATA22 binds ssDNA faster and more stably, promoting ssDNA condensation. The hMEIOB-hSPATA22 heterodimer displays strong binding affinity and stability. Multiple heterodimers spontaneously aggregate in vitro, with BLI response signals of ~4.31 nm for hSPATA22 alone versus ~19.5 nm for the heterodimer, indicating polymer formation. The hRPA complex weakens the binding affinity of hMEIOB, hSPATA22, and the heterodimer to ssDNA, and binds to hSPATA22 and the heterodimer in vitro, consistent with RPA's role in protecting ssDNA and recruiting repair proteins. This study provides the first single-molecule elucidation of hMEIOB and hSPATA22 binding to ssDNA and verifies their relationship with the RPA complex.