ObjectiveTo investigate the efficacy and safety of stereotactic body radiotherapy （SBRT） combined with sintilimab and bevacizumab in the treatment of patients with unresectable hepatocellular carcinoma （uHCC） and related prognostic factors. MethodsA total of 42 patients with uHCC who underwent SBRT combined with sintilimab and bevacizumab in Department of Radiation Oncology， The Fifth Medical Centre of PLA General Hospital， from March to December 2022 were enrolled. The prescribed dose of planning target volume was 36‍ ‍—‍ ‍50 Gy in 5‍ ‍—‍ ‍6 fractions for continuous irradiation， followed by the regimen of sintilimab and bevacizumab. Each course of treatment was 3 weeks until the presence of tumor progression or serious adverse events. The Kaplan-Meier method was used to calculate overall survival （OS） rate and progression-free survival （PFS） rate， and the log-rank test was used for comparison between groups； the Cox proportional hazards model was used to investigate the influencing factors for prognosis. ResultsThe median follow-up time was 21.6 months， with an objective response rate of 69%， a disease control rate of 85.7%， a median PFS of 10.0 months （95% confidence interval ［CI］： 6.7‍ ‍—‍ ‍13.0）， and a median OS of 23.3 months （95%CI： 14.7‍ ‍—‍ ‍31.8）. Most adverse events were grade 1‍ ‍—‍ ‍2 events， and there were no fatal adverse events. At 6‍ ‍—‍ ‍8 weeks after treatment， the AFP response group had a significantly better OS than the non-AFP response group （not reached vs 11.8 months， P=0.007）. The multivariate analysis showed that AFP response was associated with the good prognosis of patients （hazard ratio=0.31， 95%CI： 0.13‍ ‍—‍ ‍0.75， P=0.009）. ConclusionFor patients with uHCC， SBRT combined with sintilimab and bevacizumab can improve survival with a manageable safety profile， and a >50% reduction in AFP at 6‍ ‍—‍ ‍8 weeks after treatment can be used as a potential prognostic indicator.

ObjectiveTo investigate the influence of histone deacetylase 3 (HDAC3) on the occurrence, development of psoriasis-like inflammation in mice, and the relative immune mechanisms. MethodsHealthy C57BL/6 mice aged 6-8 weeks were selected and randomly divided into 3 groups: control group (Control), psoriasis model group (IMQ), and HDAC3 inhibitor RGFP966-treated psoriasis model group (IMQ+RGFP966). One day prior to the experiment, the back hair of the mice was shaved. After a one-day stabilization period, the mice in Control group was treated with an equal amount of vaseline, while the mice in IMQ group was treated with imiquimod (62.5 mg/d) applied topically on the back to establish a psoriasis-like inflammation model. The mice in IMQ+RGFP966 group received intervention with a high dose of the HDAC3-selective inhibitor RGFP966 (30 mg/kg) based on the psoriasis-like model. All groups were treated continuously for 5 d, during which psoriasis-like inflammation symptoms (scaling, erythema, skin thickness), body weight, and mental status were observed and recorded, with photographs taken for documentation. After euthanasia, hematoxylin-eosin (HE) staining was used to assess the effect of RGFP966 on the skin tissue structure of the mice, and skin thickness was measured. The mRNA and protein expression levels of HDAC3 in skin tissues were detected using reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB), respectively. Flow cytometry was employed to analyze neutrophils in peripheral blood and lymph nodes, CD4⁺ T lymphocytes, CD8⁺ T lymphocytes in peripheral blood, and IL-17A secretion by peripheral blood CD4⁺ T lymphocytes. Additionally, spleen CD4⁺ T lymphocyte expression of HDAC3, CCR6, CCR8, and IL-17A secretion levels were analyzed. Immunohistochemistry was used to detect the localization and expression levels of HDAC3, IL-17A, and IL-10 in skin tissues. ResultsCompared with the Control group, the IMQ group exhibited significant psoriasis-like inflammation, characterized by erythema, scaling, and skin wrinkling. Compared with the IMQ group, RGFP966 exacerbated psoriasis-like inflammatory symptoms, leading to increased hyperkeratosis. The psoriasis area and severity index (PASI) skin symptom scores were higher in the IMQ group than those in the Control group, and the scores were further elevated in the IMQ+RGFP966 group compared to the IMQ group. Skin thickness measurements showed a trend of IMQ+RGFP966>IMQ>Control. The numbers of neutrophils in the blood and lymph nodes increased sequentially in the Control, IMQ, and IMQ+RGFP966 groups, with a similar trend observed for CD4⁺ and CD8⁺ T lymphocytes in the blood. In skin tissues, compared with the Control group, the mRNA and protein levels of HDAC3 decreased in the IMQ group, but RGFP966 did not further reduce these expressions. HDAC3 was primarily located in the nucleus. Compared with the Control group, the nuclear HDAC3 content decreased in the skin tissues of the IMQ group, and RGFP966 further reduced nuclear HDAC3. Compared with the Control and IMQ groups, RGFP966 treatment decreased HDAC3 expression in splenic CD4⁺ and CD8⁺ T cells. RGFP966 treatment increased the expression of CCR6 and CCR8 in splenic CD4⁺ T cells and enhanced IL-17A secretion by peripheral blood and splenic CD4⁺ T lymphocytes. Additionally, compared with the IMQ group, RGFP966 reduced IL-10 protein levels and upregulated IL-17A expression in skin tissues. ConclusionRGFP966 exacerbates psoriatic-like inflammatory responses by inhibiting HDAC3, increasing the secretion of the cytokine IL-17A, and upregulating the expression of chemokines CCR8 and CCR6.

ObjectiveTo investigate the mechanism of kidney-tonifying and liver-regulating cyclical therapy and its formula in regulating endometrial receptivity during the "implantation window" in rats with polycystic ovary syndrome （PCOS）. MethodsSix rats were randomly selected from 36 SPF SD female rats as the normal group， and the remaining rats were administered letrozole to induce a PCOS model. By using a random number method， the rats were divided into the following groups： normal group， model group， Xiaoyaosan group （11.97 g·kg^-1）， Sanzi Yangmo decoction group （28.35 g·kg^-1）， cyclical therapy group （11.97/28.35 g·kg^-1）， and aspirin group （8 × 10^-3 mg·kg^-1）. After 12 days of continuous administration by gavage （equivalent to three estrous cycles）， female and male rats were co-housed. On the fifth day of pregnancy， the number of blastocyst implantation in each group was counted. Hematoxylin-eosin （HE） staining was used to observe the pathological morphology of rat endometrial tissue. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of estradiol （E₂） and progesterone （P） in rat serum. Western blot was used to detect the protein expression of vascular endothelial growth factor （VEGF）， progesterone receptor （PR）， estrogen receptor （ER）， androgen receptor （AR）， and integrin（ITG） αvβ3 in rat endometrial blood vessels. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of miR-140-5 P， VEGF， vascular endothelial growth factor receptor 2 （VEGFR2）， PR， ER， AR， and ITGαvβ3 in rat endometrium. ResultsCompared with normal group， the estrous cycle of the rats in model group continued to be in the estrus interval and the estrous cycle lost regular changes. The endometrium was significantly thinner， the number of uterine glands and blood vessels were significantly reduced （P<0.01）， and the pregnancy rate was significantly reduced. Compared with the model group， each drug group restored the regular estrous cycle to varying degrees， and the endometrial thickness and the number of blood vessels were significantly improved （P<0.01）. The pregnancy rate of each drug group increased， and the effect of the cycle therapy group could reach the normal level. The results of molecular biology experiments showed that compared with the normal group， the levels of serum E₂ and P in the model group were significantly decreased （P<0.01）， the expression of VEGF， ER， PR and ITGαvβ3 protein was significantly decreased （P<0.05，P<0.01）， the expression of AR protein was significantly increased （P<0.01）， the expression of miR-140-5P and AR mRNA was significantly increased （P<0.01）， and the expression of VEGF， VEGFR2， ER， PR and ITGαvβ3 mRNA was significantly decreased （P<0.01）. Compared with model group， the serum E₂ level in the Xiaoyaosan group was significantly increased （P<0.01）.The levels of E₂ and P in serum of rats in Sanzi Yangmo decoction group， cycle therapy group and aspirin group were significantly increased （P<0.01）. The expression of AR protein in each drug group was significantly decreased （P<0.01）. The expression of VEGF and ITGαvβ3 protein in Xiaoyaosan group was significantly increased （P<0.01）. The expression of VEGF， ER and PR protein in Sanzi Yangmo decoction group was increased to varying degrees （P<0.05，P<0.01）. The expression of VEGF， PR， ER and ITGαvβ3 protein in the cycle therapy group and the aspirin group increased to varying degrees （P<0.05，P<0.01）. The expression of miR-140-5P and AR mRNA in each drug group was significantly decreased （P<0.01）. The expression of VEGF， VEGFR2， ER， PR and ITGαvβ3 mRNA in each drug group increased to varying degrees （P<0.05，P<0.01）. Compared with Xiaoyaosan group and Sanzi Yangmo decoction group， the expression of miR-140-5P， VEGFR2， ER， PR， AR and ITGαvβ3 mRNA in the cycle therapy group were significantly different （P<0.05，P<0.01）. ConclusionThe kidney-tonifying and liver-regulating cyclical therapy may reduce the activity of miR-140-5P， target the upregulation of VEGF expression， mediate angiogenesis， and promote endometrial angiogenesis， thereby playing a synergistic role in improving endometrial receptivity in PCOS-induced infertility. Its efficacy in increasing pregnancy rates surpasses that of Xiaoyaosan or Sanzi Yangmo decoction used alone.

ObjectiveTo investigate the mechanism of kidney-tonifying and liver-regulating cyclical therapy and its formula in regulating endometrial receptivity during the "implantation window" in rats with polycystic ovary syndrome （PCOS）. MethodsSix rats were randomly selected from 36 SPF SD female rats as the normal group， and the remaining rats were administered letrozole to induce a PCOS model. By using a random number method， the rats were divided into the following groups： normal group， model group， Xiaoyaosan group （11.97 g·kg^-1）， Sanzi Yangmo decoction group （28.35 g·kg^-1）， cyclical therapy group （11.97/28.35 g·kg^-1）， and aspirin group （8 × 10^-3 mg·kg^-1）. After 12 days of continuous administration by gavage （equivalent to three estrous cycles）， female and male rats were co-housed. On the fifth day of pregnancy， the number of blastocyst implantation in each group was counted. Hematoxylin-eosin （HE） staining was used to observe the pathological morphology of rat endometrial tissue. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of estradiol （E₂） and progesterone （P） in rat serum. Western blot was used to detect the protein expression of vascular endothelial growth factor （VEGF）， progesterone receptor （PR）， estrogen receptor （ER）， androgen receptor （AR）， and integrin（ITG） αvβ3 in rat endometrial blood vessels. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of miR-140-5 P， VEGF， vascular endothelial growth factor receptor 2 （VEGFR2）， PR， ER， AR， and ITGαvβ3 in rat endometrium. ResultsCompared with normal group， the estrous cycle of the rats in model group continued to be in the estrus interval and the estrous cycle lost regular changes. The endometrium was significantly thinner， the number of uterine glands and blood vessels were significantly reduced （P<0.01）， and the pregnancy rate was significantly reduced. Compared with the model group， each drug group restored the regular estrous cycle to varying degrees， and the endometrial thickness and the number of blood vessels were significantly improved （P<0.01）. The pregnancy rate of each drug group increased， and the effect of the cycle therapy group could reach the normal level. The results of molecular biology experiments showed that compared with the normal group， the levels of serum E₂ and P in the model group were significantly decreased （P<0.01）， the expression of VEGF， ER， PR and ITGαvβ3 protein was significantly decreased （P<0.05，P<0.01）， the expression of AR protein was significantly increased （P<0.01）， the expression of miR-140-5P and AR mRNA was significantly increased （P<0.01）， and the expression of VEGF， VEGFR2， ER， PR and ITGαvβ3 mRNA was significantly decreased （P<0.01）. Compared with model group， the serum E₂ level in the Xiaoyaosan group was significantly increased （P<0.01）.The levels of E₂ and P in serum of rats in Sanzi Yangmo decoction group， cycle therapy group and aspirin group were significantly increased （P<0.01）. The expression of AR protein in each drug group was significantly decreased （P<0.01）. The expression of VEGF and ITGαvβ3 protein in Xiaoyaosan group was significantly increased （P<0.01）. The expression of VEGF， ER and PR protein in Sanzi Yangmo decoction group was increased to varying degrees （P<0.05，P<0.01）. The expression of VEGF， PR， ER and ITGαvβ3 protein in the cycle therapy group and the aspirin group increased to varying degrees （P<0.05，P<0.01）. The expression of miR-140-5P and AR mRNA in each drug group was significantly decreased （P<0.01）. The expression of VEGF， VEGFR2， ER， PR and ITGαvβ3 mRNA in each drug group increased to varying degrees （P<0.05，P<0.01）. Compared with Xiaoyaosan group and Sanzi Yangmo decoction group， the expression of miR-140-5P， VEGFR2， ER， PR， AR and ITGαvβ3 mRNA in the cycle therapy group were significantly different （P<0.05，P<0.01）. ConclusionThe kidney-tonifying and liver-regulating cyclical therapy may reduce the activity of miR-140-5P， target the upregulation of VEGF expression， mediate angiogenesis， and promote endometrial angiogenesis， thereby playing a synergistic role in improving endometrial receptivity in PCOS-induced infertility. Its efficacy in increasing pregnancy rates surpasses that of Xiaoyaosan or Sanzi Yangmo decoction used alone.

ObjectiveTo observe the effect of Yifei Jianpi prescription on the of signal transducer and activator of transcription protein 1 （STAT1）/interferon regulatory factor 3 （IRF3） signaling pathway in a pneumonia model induced by lipopolysaccharide （LPS） and to explore the mechanism of Yifei Jianpi prescription in improving lung immune and inflammatory responses. MethodsSixty male SPF SD rats were used in this study. Ten rats were randomly assigned to the normal control group， and the remaining 50 were instilled with LPS in the trachea to establish a pneumonia model. After successful modeling， the rats were randomly divided into the model group， dexamethasone group （0.5 mg·kg^-1）， and Yifei Jianpi prescription high-dose （12 mg·kg^-1）， medium-dose （6 mg·kg^-1）， and low-dose （3 mg·kg^-1） groups， with 10 rats in each group. Treatment was administered once daily， and the normal control and model groups received the same volume of normal saline. After 14 days， flow cytometry was used to detect the classification of whole blood lymphocytes. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum levels of immunoglobulin G （IgG）， immunoglobulin A （IgA）， immunoglobulin M （IgM）， and the content of tumor necrosis factor-α （TNF-α）， interleukin-8 （IL-8）， interleukin-6 （IL-6）， and interleukin-10 （IL-10） in alveolar lavage fluid （BALF）. Hematoxylin-eosin （HE） staining was used to observe lung tissue pathology and score the damage. Thymus weight， spleen weight， and wet-to-dry weight ratio （W/D） were recorded. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of STAT1， IRF3， IL-6， and interferon-alpha （IFN-α） in lung tissues， while Western blot was performed to assess the protein expression of STAT1， IRF3， IL-6， and IFN-α. ResultsCompared with the normal control group， the model group showed significantly increased proportion of B lymphocytes in peripheral blood， decreased proportions of NK cells and CD4⁺/CD8⁺ （P<0.05， P<0.01）， decreased serum levels of IgG and IgA， significantly increased IgM levels （P<0.01）， significantly elevated content of TNF-α， IL-6， and IL-8 in BALF， and significantly decreased IL-10 levels （P<0.01）. Lung tissue damage was evident， with significant increases in thymus and spleen weights and a higher W/D ratio （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly upregulated （P<0.05，P<0.01）. Compared with the model group， the Yifei Jianpi prescription groups showed significantly reduced proportions of B lymphocytes in peripheral blood， increased proportions of NK cells and CD4⁺/CD8⁺ ratios （P<0.05， P<0.01）， significantly increased serum levels of IgG and IgA， significantly decreased IgM levels （P<0.05， P<0.01）， significantly reduced levels of TNF-α， IL-6， and IL-8 in BALF， and significantly increased IL-10 levels （P<0.01）. Lung tissue damage was alleviated， thymus and spleen weights were significantly reduced， and the W/D ratio was markedly decreased （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly downregulated （P<0.05， P<0.01）. ConclusionYifei Jianpi prescription can alleviate lung tissue damage and improve immune and inflammatory responses in LPS-induced pneumonia rats. The mechanism may be related to the inhibition of STAT1/IRF3 signaling pathway activation.

Through a comprehensive analysis combining network pharmacology prediction and transcriptomics, this study systematically explained the multi-target mechanism of Cyanotis arachnoidea(CA) Gel in improving melasma. A melasma model was induced in female SD rats by progesterone injection combined with ultraviolet B(UVB) irradiation for 40 consecutive days, while the blank control group was only fed routinely. After successful model establishment, the rats were randomly divided into five groups and administered different doses of CA ethanol extract gel(high, medium, and low doses) or arbutin Gel(positive control), which were applied once daily for 28 consecutive days. Subsequently, the levels of superoxide dismutase(SOD), malondialdehyde(MDA), and tyrosinase(TYR) in the skin, serum, and liver tissues were measured. Hematoxylin-eosin(HE) staining and Masson-Fontana staining were used to observe the pathological changes in the tissues. Network pharmacology combined with transcriptomics was employed to identify core targets and pathways, and the differential gene expression was validated by quantitative real-time PCR(qPCR). Pharmacodynamic experiments showed that CA Gel significantly increased SOD activity and decreased MDA and TYR levels in the skin, serum, and liver of model rats. It also improved epidermal thickening, inflammatory infiltration, collagen loss, and melanin deposition. Network pharmacology analysis showed that CA mainly regulated core targets such as signal transducer and activator of transcription 3(STAT3), epidermal growth factor receptor(EGFR), and interleukin-6(IL-6), and modulated the phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT) and interleukin-17(IL-17) signaling pathways. Transcriptomic analysis showed that CA Gel significantly downregulated the gene expression of heat shock protein 90β family member 1(Hsp90b1), heat shock protein 90α family member 1(Hsp90aa1), and the key steroid synthesis enzyme cytochrome P450 family 17 subfamily A member 1(Cyp17a1), while upregulating thioredoxin 1(Txn1). qPCR results confirmed that CA Gel regulated oxidative stress and inflammatory response by inhibiting the IL-17 signaling pathway and steroid hormone synthesis. This study, for the first time, reveals the molecular mechanism of CA Gel in improving melasma through multi-target synergistic regulation of oxidative stress, inflammatory response, and hormone metabolism pathways, providing a scientific basis for the treatment of pigmentation diseases with traditional Chinese medicine.
Animals ; Rats ; Female ; Rats, Sprague-Dawley ; Network Pharmacology ; Drugs, Chinese Herbal/administration & dosage* ; Melanosis/metabolism* ; Transcriptome/drug effects* ; Humans ; Superoxide Dismutase/genetics* ; Signal Transduction/drug effects* ; Malondialdehyde/metabolism*

Objective: To analyze the HLA typing and STR loci chimerism in a patient with recurrent acute lymphoblastic leukemia after HLA-haploidentical hematopoietic stem cell transplantation. Methods: HLA typing was performed on peripheral blood, buccal swabs and saliva samples after transplantation using PCR-sequence-specific oligonucleotide probes (PCR-SSOP) and next-generation sequencing (NGS). Additionally, STR analysis was conducted on these samples using a 21-locus STR assay kit to detect STR loci. Results: The HLA typing and STR locus outcomes of the patient's peripheral blood and the second saliva sample post-transplantation were in full concordance with the test results of the donor (father), whereas the HLA typing and STR locus results derived from the buccal swabs and the first saliva sample indicated chimerism between the donor and the recipient. Conclusion: In the follow-up and monitoring after transplantation, apart from focusing on peripheral blood samples, it is recommended to regularly monitor HLA typing and STR loci chimerism in patients' buccal swabs and saliva samples to comprehensively evaluate the transplantation effect and recurrence risk.

Objective: To analyze the HLA typing and STR loci chimerism in a patient with recurrent acute lymphoblastic leukemia after HLA-haploidentical hematopoietic stem cell transplantation. Methods: HLA typing was performed on peripheral blood, buccal swabs and saliva samples after transplantation using PCR-sequence-specific oligonucleotide probes (PCR-SSOP) and next-generation sequencing (NGS). Additionally, STR analysis was conducted on these samples using a 21-locus STR assay kit to detect STR loci. Results: The HLA typing and STR locus outcomes of the patient's peripheral blood and the second saliva sample post-transplantation were in full concordance with the test results of the donor (father), whereas the HLA typing and STR locus results derived from the buccal swabs and the first saliva sample indicated chimerism between the donor and the recipient. Conclusion: In the follow-up and monitoring after transplantation, apart from focusing on peripheral blood samples, it is recommended to regularly monitor HLA typing and STR loci chimerism in patients' buccal swabs and saliva samples to comprehensively evaluate the transplantation effect and recurrence risk.

ObjectiveThis study explores the methods of lung tissue extraction and fixation required for pathological studies of fetal rats, based on the unique physiological structure of fetal rat lung tissue and existing lung tissue fixation techniques for adult rats. MethodsSix pregnant adult SD rats at 20.5 days of gestation were subjected to cesarean section to obtain fetal rats. Four healthy fetal rats with similar body weight, vital signs, and respiratory status were selected from each pregnant rat, and they were randomly divided into the following groups using a random number table: direct lung infiltration group, lung infiltration group after intratracheal infusion, whole-body infiltration group of fetal rats, and whole-body infiltration group after intratracheal infusion of fetal rats. To systematically compare and analyze the anatomical morphology under different fixation methods, lung tissues from four groups of fetal rats were harvested, perfused, and fixed, and the gross morphology of lung tissues in each group was observed. Paraffin sections were prepared and stained with Hematoxylin-Eosin (H&E). The histological morphology of the whole lung, alveoli, and bronchi was further examined under optical microscopy. ResultsIn the direct lung infiltration group, the hilar structures were unclear, lung lobation was indistinct, the shape was irregular, lung cavities were small, and alveoli and bronchi were shrunken. In the lung infiltration group after intratracheal infusion, the hilar structures were clear, lobation was pronounced, the shape was regular, lung cavities were large, and alveoli and bronchi were full. Both the whole-body infiltration group and whole-body infiltration group after intratracheal infusion of fetal rats exhibited visible lungs, hearts, skins, and other organs. The lung tissues of both groups showed obvious lobulation, irregular shape, and damage at the margins of lung lobes. In the whole-body infiltration group, the thoracic cavities of the fetus were flattened, lung cavities were small, and alveoli and bronchi were shrunken. In the whole-body infiltration group after intratracheal infusion of fetal rats, the fetal thoracic cavities were full, lung cavities were large, and alveoli and bronchi were relatively full. ConclusionThe lung infiltration after intratracheal infusion method for fetal rat lung tissue fixation outperforms direct lung infiltration, whole-body infiltration of fetal rats, and whole-body infiltration after intratracheal infusion of fetal rats in terms of preservation of the lung tissue's original morphology, paraffin sectioning, staining, and pathological observation and analysis. The embedding, sectioning, and staining processes are also simple and save consumables. Therefore, intratracheal infusion followed by lung infiltration method is recommended for fixation in histopathological observation of fetal rat lung tissue.

Rheumatoid arthritis (RA) represents a persistent autoimmune condition distinguished by a multifaceted etiology that encompasses both genetic and environmental factors. Recent progress in understanding the mechanisms behind RA pathogenesis has delved into the critical role of epigenetic regulatory processes, including DNA methylation, histone modifications, and the regulation by microRNAs (miRNAs). These findings provide new insights into the intricate nature of RA and pave the way for innovative therapeutic strategies. This review consolidates the latest developments in the epigenetic regulation of RA, concentrating on how these mechanisms affect the dysregulated signaling pathways associated with the disease. We analyze the roles of specific proteins that function as 'writers', 'erasers', and 'readers' in epigenetic modifications, highlighting their potential as targets for therapeutic intervention. Additionally, in view of the significance of miRNAs in the pathogenesis of RA, we deliberate on their involvement in disease progression and explore miRNA-based treatment strategies. By integrating these diverse epigenetic dimensions, this review offers a comprehensive epigenetic perspective on RA pathogenesis and identifies promising avenues for future research and therapeutic interventions.