Ameliorative effects of mesenchymal stromal cells on senescence associated phenotypes in naturally aged rats.

BACKGROUND: Aging is a multifaceted process that affects all organ systems. With the increasing trend of population aging, aging-related diseases have resulted in significant medical challenges and socioeconomic burdens. Mesenchymal stromal cells (MSCs), due to their antioxidative stress, immunoregulatory, and tissue repair capabilities, hold promise as a potential anti-aging intervention. METHODS: In this study, we transplanted MSCs into naturally aged rats at 24 months, and subsequently examined levels of aging-related factors such as ß-galactosidase, superoxide dismutase, p16, p21 and malondialdehyde in multiple organs. Additionally, we assessed various aging-related phenotypes in these aged rats, including immune senescence, lipid deposition, myocardial fibrosis, and tissue damage. We also conducted a 16 S ribosomal ribonucleic acid (rRNA) analysis to study the composition of gut microbiota. RESULTS: The results indicated that MSCs significantly reduced the levels of aging-associated and oxidative stress-related factors in multiple organs such as the heart, liver, and lungs of naturally aging rats. Furthermore, they mitigated chronic tissue damage and inflammation caused by aging, reduced levels of liver lipid deposition and myocardial fibrosis, alleviated aging-associated immunodeficiency and immune cell apoptosis, and positively influenced the gut microbiota composition towards a more youthful state. This research underscores the diverse anti-aging effects of MSCs, including oxidative stress reduction, tissue repair, metabolic regulation, and improvement of immune functions, shedding light on the underlying anti-aging mechanisms associated with MSCs. CONCLUSIONS: The study confirms that MSCs hold great promise as a potential anti-aging approach, offering the possibility of extending lifespan and improving the quality of life in the elderly population.

Immunotherapy in the context of sepsis-induced immunological dysregulation.

Sepsis is a clinical syndrome caused by uncontrollable immune dysregulation triggered by pathogen infection, characterized by high incidence, mortality rates, and disease burden. Current treatments primarily focus on symptomatic relief, lacking specific therapeutic interventions. The core mechanism of sepsis is believed to be an imbalance in the host's immune response, characterized by early excessive inflammation followed by late immune suppression, triggered by pathogen invasion. This suggests that we can develop immunotherapeutic treatment strategies by targeting and modulating the components and immunological functions of the host's innate and adaptive immune systems. Therefore, this paper reviews the mechanisms of immune dysregulation in sepsis and, based on this foundation, discusses the current state of immunotherapy applications in sepsis animal models and clinical trials.

Elevated Ozone Reduces the Quality of Tea Leaves but May Improve the Resistance of Tea Plants.

Tropospheric ozone (O3) pollution can affect plant nutritional quality and secondary metabolites by altering plant biochemistry and physiology, which may lead to unpredictable effects on crop quality and resistance to pests and diseases. Here, we investigated the effects of O3 (ambient air, Am; ambient air +80 ppb of O3, EO3) on the quality compounds and chemical defenses of a widely cultivated tea variety in China (Camellia sinensis cv. 'Baiye 1 Hao') using open-top chamber (OTC). We found that elevated O3 increased the ratio of total polyphenols to free amino acids while decreasing the value of the catechin quality index, indicating a reduction in leaf quality for green tea. Specifically, elevated O3 reduced concentrations of amino acids and caffeine but shows no impact on the concentrations of total polyphenols in tea leaves. Within individual catechins, elevated O3 increased the concentrations of ester catechins but not non-ester catechins, resulting in a slight increase in total catechins. Moreover, elevated O3 increased the emission of biogenic volatile organic compounds involved in plant defense against herbivores and parasites, including green leaf volatiles, aromatics, and terpenes. Additionally, concentrations of main chemical defenses, represented as condensed tannins and lignin, in tea leaves also increased in response to elevated O3. In conclusion, our results suggest that elevated ground-level O3 may reduce the quality of tea leaves but could potentially enhance the resistance of tea plants to biotic stresses.

Delta-SVV as a Predictor for Circulating Blood Volume Evaluation during Intraoperative Period: A Prospective Cohort Study.

Background: Precise fluid therapy is extremely important during surgeries, as enough circulating blood volume ensures tissue perfusion and cell oxygenation. Yet, extra fluid volume could cause other adverse events, such as heart failure, intestinal swelling, etc. Thus, precise evaluation of the circulating blood volume is essential for maintaining sufficient circulating blood volume and avoiding excessive fluid infusion. Objective: This study aimed to evaluate the relationship between SVV and circulating blood volume during intraoperative fluid therapy. Methods: SVV was measured by FloTrac/Vigileo in the study. A prospective cohort study was conducted. 103 patients aged from 20 to 60 years old with an ASA Grade I-II and a diagnosis of meningioma less than 3 centimeters planning for selective neurosurgery were randomly divided into the Crystalloid Group and the Colloid Group. After induction, each Patient received 15 ml/kg of Plasma-Lyte-A or 6% hydroxyethyl starch in 30 min followed by continuous infusion at the speed of 0.1 ml/kg during the next 60 min. Hb concentration, Hct, Delta-BV/kg, and Delta-SVV were recorded every 5 minutes. Results: The delta-SVV and Delta-bv/kg were significantly higher in the Crystalloid Group than that of the Colloid Group. There was a strong linear correlation between Delta-SVV and Delta-bv/kg in both Crystalloid Group (Delta-bv / kg = 1.108 Delta-SVV + 0.0712, P < .001) and Colloid Group (Delta-bv / kg = 1.047 Delta-SVV + 0.4153, P < .001). An equation between Delta-bv/kg and Delta-SVV was established (Delta-bv / kg = 1.099 Delta-SVV + 0.1139, P < .001). Conclusion: In conclusion, SVV measured by FloTrac / Vigileo could guile fluid therapy precisely by predicting the blood volume of patients during the intraoperative period, as it has a strong linear correlation with the blood volume of patients who underwent general anesthesia, meaning anesthesiologist could calculate the exact fluid volume for patients' infusion. Further studies with large cohorts and centers would be needed to validate its efficiency.

Expression and Correlation of HER2/P53/VEGF in Marjolin's Ulcer.

Marjolin's ulcer is described as malignant lesions developed in the injured skin, which can cause several kinds of malignancies. Our results showed that no HER2 but p53 was detected in Majorlin's ulcer samples. Meanwhile, by statistical analysis, we found that the positive rate of p53 in Majorlin's ulcer samples was associated with the pathological type of ulcer canceration and degree of tumor differentiation. The positive expression rate of vascular endothelial growth factor (VEGF) was 62.5% in poorly differentiated squamous cell carcinoma (SCC), 39.4% in moderately differentiated SCC, and 66.7% in well-differentiated SCC, respectively. Furthermore, some cases of Majorlin's ulcer with positive P53 were negative for VEGF, while some cases with positive VEGF were negative for P53. Image superposition showed that VEGF expression was absent or minimal in p53-positive cases. However, P53 was not expressed or rarely expressed in VEGF-positive cases. Our results of this study will suggest that P53 can be used as the mark of Marjolin's ulcer differentiation, and there may be some interaction between P53 and VEGF in Marjolin's ulcer. The regulation of microenvironment in the oncogenesis, progression, and differentiation of Marjolin's ulcer is complex and needs further study.

Spatiotemporal Dynamics of Phthalate Esters in Tea Plants Growing Different Geographical Environments and an Attempt on Their Risk Assessment.

The phthalate esters (PAEs) have become ubiquitous pollutants. In the present work, we investigated their pollution on teas. Dimethyl phthalate (DMP), diethyl phthalate (DEP), diisobutyl phthalate (DiBP), di-n-butyl phthalate (DBP), and di-(2-ethyl) hexyl phthalate (DEHP) were detected in all fresh tea leaves with DBP being the major congener of PAEs in teas followed by DiBP and DEHP. Seasonal variation, spatial distribution difference, correlationship of environmental factors, and potential health risks of PAEs were analyzed. The PAEs content in one bud and two leaves was lower than that in upper mature leaves in tea plants. The PAEs content in fresh tea leaves was the lowest in spring, while it was high in autumn and winter. The correlation analysis results showed that PAEs had significantly negative correlation with ambient air temperature, while it was positively correlated with the air quality index. PAEs analysis of spring tea in Anhui and Zhejiang provinces further indicated that the factor of provincial regions had little impact on the PAEs pollution level in tea. By contrast, the different environmental areas significantly affected PAE pollution, especially the agricultural areas. The human daily intake-based (13 g/day) risk assessment indicated that both the carcinogenic and non-carcinogenic risks (1.76 × 10-7-6.12 × 10-7) of PAEs via tea consumption were acceptable, with the estrogen equivalence (1.60-6.29 ng E2/kg) being at a medium level. This study provides significant information for pollution control and risk assessment of PAEs in Chinese tea production.

A new border for circadian rhythm gene NFIL3 in diverse fields of cancer.

The circadian rhythm disorder and abnormal expression of rhythm genes are related to many diseases, especially cancer. Rhythm gene NFIL3 is involved in energy metabolism and immune cell differentiation, and its aberrant expression is associated with metabolic diseases and inflammation. Previously, numerous studies have shown that aberrant NFIL3 expression is associated with tumorigenesis, progression, and chemotherapy resistance. For instance, NFIL3 performs as a nuclear transcription factor, impacts cell proliferation, represses apoptosis, and promotes cancer cell invasion and metastasis by regulating the transcription of target genes. In addition, NFIL3 expressed in cancer cells influences the type and proportion of infiltrated immune cells in the tumor microenvironment. Increased expression of NFIL3 induces the chemotherapy and immunotherapy resistance in cancer. In this review, we summarized the pathological functions of NFIL3 in tumorigenesis, cancer development, and treatment. The rhythm gene NFIL3 can be used as a promising target in cancer therapy in the future.

The long non-coding RNA lncMYOZ2 mediates an AHCY/MYOZ2 axis to promote adipogenic differentiation in porcine preadipocytes.

Long non-coding RNAs (lncRNAs) play a vital role in regulating adipogenesis. However, the associated regulatory mechanisms have yet to be described in detail in pig. In this study, we demonstrate a critical role for lncMYOZ2 in adipogenesis from porcine preadipocytes. Specifically, lncMYOZ2 was more abundant in the adipose tissue of Mashen (fat-type) pigs than for Large White (lean-type) pigs, and knockdown of this lncRNA significantly inhibited the differentiation of porcine preadipocytes into adipocytes. Mechanistically, we used RNA pull-down and RIP assays to establish that lncMYOZ2 interacts with adenosylhomocysteinase (AHCY). Moreover, lncMYOZ2 knockdown increased promoter methylation of the target gene MYOZ2 and lowered its expression. Finally, we describe a positive regulatory role for MYOZ2 in adipogenesis. Collectively, these findings establish lncMYOZ2 as an important epigenetic regulator of adipogenesis via the aforementioned AHCY/MYOZ2 pathway, and provide insights into the role of lncRNAs in porcine adipose development.

Notoginsenoside R1 suppresses inflammatory response and the pyroptosis of nucleus pulposus cells via inactivating NF-κB/NLRP3 pathways.

Intervertebral disc degeneration (IVDD) is the main cause of low back pain. Notoginsenoside R1 (NR1) is widely applied in the treatment of bone disorders, including IVDD. The present study aimed to investigate the effects of NR1 on the development of IVDD and the potential mechanisms. AF puncture was performed to establish IVDD rat model. Histology changes were analyzed by hematoxylin and eosin (H&E) staining. mRNA expressions were determined using qRT-PCR. Protein expressions were detected with western blot. Cellular functions were detected by MTT, EdU, flow cytometry, and TUNEL assays. The results showed that NR1 suppressed AF puncture induced IVDD, restored intervertebral disc (IVD) function, and suppressed mechanical hyperalgesia and thermal hyperalgesia. Moreover, NR1 promoted the release of extracellular matrix (ECM) in vivo and in vitro, and decreased the mRNA expressions of proinflammation cytokines. Additionally, NR1 inactivated NF-κB/NLRP3 pathways, improved cellular functions of nucleus pulposus cells (NPCs), and suppressed cell pyroptosis, which was reversed by NLRP3 activation. Taken together, NR1 may protect against IVDD via suppressing NF-κB/NLRP3 pathways. This may provide a novel therapy for IVDD.

Corrigendum to "EF24 Suppresses Invasion and Migration of Hepatocellular Carcinoma Cells In Vitro via Inhibiting the Phosphorylation of Src".

[This corrects the article DOI: 10.1155/2016/8569684.].

Hypoxia-Induced LIN28A mRNA Promotes the Metastasis of Colon Cancer in a Protein-Coding-Independent Manner.

The hypoxic microenvironment is beneficial to the metastasis but not to the proliferation of cancer cells. However, the mechanisms regarding to hypoxia differentially regulating cancer metastasis and proliferation are largely unknown. In this study, we revealed that hypoxia induced the expression of LIN28A at mRNA level but segregated LIN28A mRNAs in the P-bodies and thus inhibits the production of LIN28A protein. This unexpected finding suggests that there may be non-coding role for LIN28A mRNA in the progression of colon cancer. We further showed that the non-coding LIN28A mRNA promotes the metastasis but not proliferation of colon cancer cells in vitro and in vivo. Mechanistically, we revealed that methionyl aminopeptidase 2 (METAP2) is one of the up-regulated metastasis regulators upon over-expression of non-coding LIN28A identified by mass spectrum, and confirmed that it is non-coding LIN28A mRNA instead of LIN28A protein promotes the expression of METAP2. Moreover, we demonstrated that knockdown of DICER abolished the promotional effects of non-coding LIN28A on the metastasis and METAP2 expression. Conclusively, we showed that hypoxia induces the production of LIN28A mRNAs but segregated them into the P-bodies together with miRNAs targeting both LIN28A and METAP2, and then promotes the metastasis by positively regulating the expression of METAP2. This study uncovered a distinctive role of hypoxia in manipulating the metastasis and proliferation by differently regulating the expression of LIN28A at mRNA and protein level.

miR-128 regulated the proliferation and autophagy in porcine adipose-derived stem cells through targeting the JNK signaling pathway.

PURPOSE: microRNA-128 (miR-128), a brain-enriched microRNA, has been reported to play a crucial role in the treatment of diseases. The c-Jun N-terminal kinase (JNK) signaling pathway exerts various biological functions such as regulation of cell proliferation, differentiation and apoptosis. In this study, we investigated the role of the miRNA-128-JNK signaling pathway in proliferation, apoptosis and autophagy of porcine adipose-derived stem cells (ASCs). METHODS: After over-expressing miR-128 in porcine ASCs, cell proliferation was determined by 2,3-Bis-(2-Methoxy-4-Nitro-5-Sulfophenyl)-2H-Tetrazolium-5-Carboxanilide (XTT) method, cell apoptosis was observed by Flow cytometry (FCM), the expression of miR-128, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) was measured by RNA preparation and reverse transcription polymerase chain reaction (RT-PCR), and protein expression of JNK, phosphorylated JNK (p-JNK) and LC3B was analyzed by Western Blot analysis. RESULTS: The over-expression of miR-128 potently promoted cell proliferation and autophagy while suppressed the apoptosis of porcine ASCs. In addition, the down-regulated expression level of p-JNK was detected in miR-128-over-expressed porcine ASCs. However, followed by the block of the JNK signaling pathway using SP600125 inhibitor, the effects of miR-128 on the proliferation, apoptosis and autophagy of porcine ASCs were significantly suppressed. CONCLUSION: It is demonstrated that the miR-128-JNK signaling pathway is a potential therapeutic target for the treatment of obesity.

AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes.

AURKA, a cell cycle-regulated kinase, is associated with malignant transformation and progression in many cancer types. We analyzed the expression change of AURKA in pan-cancer and its effect on the prognosis of cancer patients using the TCGA dataset. We revealed that AURKA was extensively elevated and predicted a poor prognosis in most of the detected cancer types, with an exception in colon cancer. AURKA was elevated in colon cancer, but the upregulation of AURKA indicated better outcomes of colon cancer patients. Then we revealed that undermethylation of the AURKA gene and several transcription factors contributed to the upregulation of AURKA in colon cancer. Moreover, we demonstrated that AURKA overexpression promoted the death of colon cancer cells induced by Oxaliplatin, whereas knockdown of AURKA significantly weakened the chemosensitivity of colon cancer cells to Oxaliplatin. Mechanistically, AURKA inhibited DNA damage response by suppressing the expression of various DNA damage repair genes in a TP53-dependent manner, which can partly explain that ARUKA is associated with a beneficial outcome of colon cancer. This study provided a possibility to use AURKA as a biomarker to predict the chemosensitivity of colon cancer to platinum in the clinic.

Stimulator of Interferon Genes Signaling Pathway and its Role in Anti-tumor Immune Therapy.

Stimulator of interferon genes is an important innate immune signaling molecule in the body and is involved in the innate immune signal transduction pathway induced by pathogen-associated molecular patterns or damage-associated molecular patterns. Stimulator of interferon genes promotes the production of type I interferon and thus plays an important role in the innate immune response to infection. In addition, according to a recent study, the stimulator of interferon genes pathway also contributes to anti-inflammatory and anti-tumor reactions. In this paper, current researches on the Stimulator of interferon genes signaling pathway and its relationship with tumor immunity are reviewed. Meanwhile, a series of critical problems to be addressed in subsequent studies are discussed as well.

IRX5 prompts genomic instability in colorectal cancer cells.

The Iroquois homeobox gene 5 (IRX5), one of the members of the Iroquois homeobox family, has been identified to correlate with worse prognosis in many cancers, including colorectal cancer (CRC). In this study, upregulation of IRX5 revealed a great reduction in the proliferation of CRC colorectal cancer cell line SW480 and DLD-1, which was accompanied by G1/S arrest, increased expression in cyclin E1, P21, and P53 and a decrease in cyclin A2, B1, and D1. Furthermore, IRX5-mediated an increase expression of RH2A protein, the biomarker of DNA damage. Consequently, the SA-ß-gal level is higher in IRX5-overexpression cells compared to control ones, which showed elevated DNA damage triggered cellular senescence. Recapitulating the above findings, IRX5 exhibited higher levels of genomic instability. IRX5 may be a perspective target for cancer therapy and it deserves further investigation.

Blood-triggered generation of platinum nanoparticle functions as an anti-cancer agent.

Since the discovery of metal nanoparticles (NPs) in the 1960s, unknown toxicity, cost and the ethical hurdles of research in humans have hindered the translation of these NPs to clinical use. In this work, we demonstrate that Pt NPs with protein coronas are generated in vivo in human blood when a patient is treated with cisplatin. These self-assembled Pt NPs form rapidly, accumulate in tumors, and remain in the body for an extended period of time. Additionally, the Pt NPs are safe for use in humans and can act as anti-cancer agents to inhibit chemotherapy-resistant tumor growth by consuming intracellular glutathione and activating apoptosis. The tumor inhibitory activity is greatly amplified when the Pt NPs are loaded in vitro with the chemotherapeutic drug, daunorubicin, and the formulation is effective even in daunorubicin-resistant models. These in vivo-generated metal NPs represent a biocompatible drug delivery platform for chemotherapy resistant tumor treatment.

Effects of multiple antibiotics on greenhouse gas and ammonia emissions during swine manure composting.

Antibiotics are commonly used in intensive farming, leading to multiple antibiotic residue in livestock waste. However, the effects of multiple antibiotics on the emissions of greenhouse gas and ammonia remain indistinct. This paper selects sulfamethoxazole and norfloxacin to represent two different types of antibiotics to explore their effects on gaseous emissions. Four treatments including CK (control), SMZ (spiked with 5 mg kg-1 DW sulfamethoxazole), NOR (spiked with 5 mg kg-1 DW norfloxacin), and SN (spiked with 5 mg kg-1 DW sulfamethoxazole and 5 mg kg-1 DW norfloxacin) were composted for 65 days. Coexistence of sulfamethoxazole and norfloxacin facilitated the biodegradation of organic carbon, and significantly (p < 0.05) increased the cumulative CO2 emission by 31.9%. The cumulative CH4 emissions were decreased by 6.19%, 23.7%, and 27.6% for SMZ, NOR, and SN, respectively. The total NH3 volatilization in SMZ and NOR rose to 1020 and 1190 mg kg-1 DW, respectively. The individual existence of sulfamethoxazole significantly (p < 0.05) ascended the N2O emission rate in the first 7 days due to the increase of NO2--N content. In addition, coexistence of sulfamethoxazole and norfloxacin notably dropped the total greenhouse gas emission (subtracting CO2) by 15.5%.

IRX5 promotes colorectal cancer metastasis by negatively regulating the core components of the RHOA pathway.

Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. As tumor metastasis is the leading cause of death in patients with CRC, it is important to elucidate the molecular mechanisms that drive CRC metastasis. Studies have shown a close relationship between Iroquois homeobox (IRX) family genes and multiple cancers, while the mechanism by which IRX5 promotes CRC metastasis is unclear. Therefore, we focused on the involvement of IRX5 in CRC metastasis. In this study, analyses of clinical data indicated that the expression of IRX5 was coincided with metastatic colorectal tumors tissues and was negatively correlated with the overall survival of patients with CRC. Functional analysis showed that IRX5 promoted the migration and invasion of CRC cells, accompanied by a large number of cellular protrusions. IRX5-overexpressing cells were more likely to form metastatic tumors in nude mice. Further analysis demonstrated that the core components of the RHOA/ROCK1/LIMK1 pathway were significantly inhibited in IRX5-overexpressing cells. Overexpression of LIMK1 effectively reversed the enhanced cellular motility caused by IRX5 overexpression. Moreover, we found that high levels of IRX5 in intestinal tissues were correlated with the inflammatory response. IRX5 was significantly increased in azoxymethane/dextran sodium sulfate intestinal tissue of mice and IRX5-overexpressing may also enhance chemokines CXCL1 and CXCL8. In summary, our findings suggested that IRX5 promoted CRC metastasis by inhibiting the RHOA-ROCK1-LIMK1 axis, which correlates with a poor prognosis.

Oncological safety of intrafascial nerve-sparing radical prostatectomy compared with conventional process: a pooled review and meta-regression analysis based on available studies.

BACKGROUND: Intrafascial prostatectomy was a modified technique from the conventional nerve-sparing surgery in order to improve patients' post-surgical continence and erectile function; however, ongoing controversy exists regarding the oncological safety of this technique. In this study we aimed to provide a critical and pooled analysis based on published literatures regarding the oncological outcomes after intrafascial nerve-sparing prostatectomy. METHODS: Database searches were performed for published articles till June 2018 on PubMed. Three reviewers screened fulfilled papers and extracted data independently. Main outcome was the positive surgical margins (PSMs) rates stratified by pathological stages. We performed both one-arm and comparative meta-analysis to evaluate the oncological safety of intrafascial technique. Moreover, we built meta-regression models to assess the confounding factors. RESULTS: We retrieved a total of 117 records after electronic search, of which 21 studies were finally included in this review. There were 15 controlled studies and 6 surgical series. Our one-arm meta-analysis demonstrated that the total PSM rates after intrafascial techniques ranging from 2.2 to 35%, with a pooled rate of 14.5% on average (480 of 3151 patients, 95% confidence interval[CI]: 11.2-17.5%). Meta-regression model showed that patients' age, pT2 cancer percentage and Selection Score of Oncological Safety (SSOS) were significantly associated with total PSM rate; moreover, each 1 point of SSOS could decrease the total PSM rate by 1.3% on average. Comparative meta-analysis demonstrated that there was no significant difference between intra- and inter-fascial group regarding PSM rates. CONCLUSIONS: With stringent case selection and when performed by experienced surgeons, intrafascial prostatectomy could offer an acceptable or, at least, equivalent PSM rate compared with the conventional interfascial approach. Preoperative SSOS more than 7 points could be considered as an indication of intrafascial radical prostatectomy.

Intrafascial nerve-sparing radical prostatectomy improves patients' postoperative continence recovery and erectile function: A pooled analysis based on available literatures.

BACKGROUND: Intrafascial nerve-sparing prostatectomy has been currently applied based on the updated anatomic understanding of periprostatic cavernous nerves, in order to provide patients better postoperative recovery of continence and potency. The aim of our study is to perform a pooled analysis of available literatures regarding the functional outcomes following intrafascial nerve-sparing technique. METHODS: The authors performed database searches of articles published till October 2017 on PubMed using following keywords across the "title" and "abstract" field of the records: intrafascial, veil, curtain dissection, high anterior release, incremental nerve sparing, and radical prostatectomy. Fulfilled papers were screened and data were extracted independently by 3 reviewers. Main outcome was the postoperative continence and potency rate stratified by follow-up durations. Both 1-arm and comparative meta-analyses were performed and meta-regression models were conducted to evaluate the confounding factors. RESULTS: Using the electronic search strategy, a total of 71 records were retrieved and 20 studies were finally included, of which 6 were surgical series and 14 were controlled studies. Our 1-arm meta-analysis summarized the pooled continence rates after intrafascial prostatectomy were 59.4%, 76.2%, 89.9%, and 92.2% at postoperative follow-up of 1, 3, 6, and 12 months, respectively. Regardless of the variance in potency definition, the pooled potency rates after intrafascial prostatectomy were 42.2%, 54.2%, and 72.2% at 3, 6, and 12 months, respectively. Comparative analysis showed that the intrafascial group offered better continence rates at 1, 3, and 6 months with an odds ratio (OR) of 2.38 (95% confidence interval [CI]: 1.73-3.26), 1.82 (95% CI: 1.18-2.82), and 2.19 (95% CI: 1.43-3.34) as compared with the interfascial group. Moreover, potency rate in the intrafascial group was higher at 12 months than in the interfascial group, with an OR of 2.44 (95% CI: 1.35-4.42). CONCLUSION: Based on the limited evidence, our study demonstrated that intrafascial nerve-sparing prostatectomy could provide patients with earlier recovery of continence and better erectile function compared with conventional interfascial approach, but physiological mechanisms about this technique still need further study.