A Phase I Clinical Study Comparing the Pharmacokinetics, Safety, and Immunogenicity of GB221 Injection and Trastuzumab (Herceptin®) in Healthy Chinese Adults.

BACKGROUND AND OBJECTIVE: GB221 is a recombinant humanized anti-HER2 monoclonal antibody. The purpose of this study was to evaluate the pharmacokinetic, safety, and immunogenicity of GB221 in healthy Chinese adults in comparison to trastuzumab (Herceptin®). METHODS: In this randomized, double-blind, parallel-group phase I clinical trial, 88 subjects were randomized 1:1 to receive a single intravenous infusion (90-100 min) of GB221 or trastuzumab (6 mg/kg). The primary pharmacokinetic parameters-maximum observed serum concentration (Cmax), area under the serum concentration-time curve from zero to the last quantifiable concentration at time t (AUC0-t), and area under the serum concentration-time curve from time zero to infinity (AUC0-∞)-of GB221 and trastuzumab were compared to establish whether the 90% confidence interval (CI) attained the 80-125% bioequivalence standard. Safety and immunogenicity were also evaluated. RESULTS: The GB221 group (n = 43) and the trastuzumab group (n = 44) showed similar pharmacokinetic characteristics. The geometric mean ratios (90% CI) of Cmax, AUC0-t, and AUC0-∞ between the two groups were 107.53% (102.25-113.07%), 108.31% (103.57-113.26%), and 108.34% (103.57-113.33%), respectively. The incidence of treatment-emergent adverse events (TEAEs) was 83.7% (36/43) of the subjects in the GB221 group and 95.5% (42/44) of the subjects in the trastuzumab group. No subjects withdrew from the trial due to TEAEs, and there were no occurrences of serious adverse events. All subjects tested negative for antidrug antibodies (ADA). CONCLUSION: GB221 demonstrated similar pharmacokinetics to trastuzumab and comparable safety and immunogenicity in healthy Chinese adults.

Adeno-associated virus-mediated gene therapy for rare pediatric neurogenetic diseases: Current status and outlook. / è ºç›¸å ³ç— æ¯’ä»‹å¯¼çš„åŸºå› æ²»ç–—åœ¨å„¿ç«¥ç¥žç»é—ä¼ ç½•è§ç— ä¸­åº”ç”¨çš„çŽ°çŠ¶ä¸Žå±•æœ›.

Rare pediatric neurogenetic diseases always have early onset, no specific therapy, high mortality, and pose a severe risk to the health and survival of children. Adeno-associated virus (AAV)-mediated gene therapy, a type of disease-modifying therapy, provides a new option for the treatment of rare pediatric neurogenetic diseases and represents a significant advancement in the field. Currently, the US Food and Drug Administration (FDA) and the European Medicines Association (EMA) have approved AAV-mediated gene therapy medications for treating spinal muscular atrophy, aromatic L-amino acid decarboxylase deficiency, and Duchenne muscular dystrophy. Numerous preclinical and clinical trial research findings from recent years indicate that AAV-mediated gene therapy has a promising future in treating genetic disorders. The quick approval process for rare diseases medications may bring hope for the treatment of children with rare neurogenetic diseases. AAV-mediated gene therapy is an emerging technology with certain risks and challenges. It is necessary to establish a standardized regulatory system and a sound long-term follow-up system to evaluate the efficacy and safety of gene therapy.

Proteomic and phosphoproteomic landscape of salivary extracellular vesicles to assess OSCC therapeutical outcomes.

Circulating extracellular vesicles (EVs) have emerged as an appealing source for surrogates to evaluate the disease status. Herein, we present a novel proteomic strategy to identify proteins and phosphoproteins from salivary EVs to distinguish oral squamous cell carcinoma (OSCC) patients from healthy individuals and explore the feasibility to evaluate therapeutical outcomes. Bi-functionalized magnetic beads (BiMBs) with Ti (IV) ions and a lipid analog, 1,2-Distearoyl-3-sn-glycerophosphoethanolamine (DSPE) are developed to efficiently isolate EVs from small volume of saliva. In the discovery stage, label-free proteomics and phosphoproteomics quantification showed 315 upregulated proteins and 132 upregulated phosphoproteins in OSCC patients among more than 2500 EV proteins and 1000 EV phosphoproteins, respectively. We further applied targeted proteomics by coupling parallel reaction monitoring with parallel accumulation-serial fragmentation (prm-PASEF) to measure panels of proteins and phosphoproteins from salivary EVs collected before and after surgical resection. A panel of three total proteins and three phosphoproteins, most of which have previously been associated with OSCC and other cancer types, show sensitive response to the therapy in individual patients. Our study presents a novel strategy to the discovery of effective biomarkers for non-invasive assessment of OSCC surgical outcomes with small amount of saliva.

HRS Regulates Small Extracellular Vesicle PD-L1 Secretion and Is Associated with Anti-PD-1 Treatment Efficacy.

PD-L1 localized to immunosuppressive small extracellular vesicles (sEV PD-L1) contributes to tumor progression and is associated with resistance to immune-checkpoint blockade (ICB) therapy. Here, by establishing a screening strategy with a combination of tissue microarray (TMA), IHC staining, and measurement of circulating sEV PD-L1, we found that the endosomal sorting complex required for transport (ESCRT) member protein hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) was the key regulator of circulating sEV PD-L1 in head and neck squamous cell carcinoma (HNSCC) patients. Increased HRS expression was found in tumor tissues and positively correlated with elevated circulating sEV PD-L1 in patients with HNSCC. The expression of HRS was also negatively correlated to the infiltration of CD8+ T cells. Knockdown of HRS markedly reduced PD-L1 expression in HNSCC cell-derived sEVs, and these sEVs from HRS knockdown cells showed decreased immunosuppressive effects on CD8+ T cells. Knockout of HRS inhibited tumor growth in immunocompetent mice together with PD-1 blockade. Moreover, a higher HRS expression was associated with a lower response rate to anti-PD-1 therapy in patients with HNSCC. In summary, our study reveals HRS, the core component of ESCRT-0, regulates sEV PD-L1 secretion, and is associated with the response to ICB therapy in patients with HNSCC, suggesting HRS is a promising target to improve cancer immunotherapy.

[Application of adeno-associated virus-mediated gene therapy in lysosomal storage diseases]. / è ºç›¸å ³ç— æ¯’ä»‹å¯¼çš„åŸºå› ç–—æ³•åœ¨æº¶é ¶ä½“è´®ç§¯ç—‡ä¸­çš„åº”ç”¨.

Lysosomal storage disorders (LSDs) are a group of single-gene inherited metabolic diseases caused by defects in lysosomal enzymes or function-related proteins. Enzyme replacement therapy is the main treatment method in clinical practice, but it has a poor effect in patients with neurological symptoms. With the rapid development of multi-omics, sequencing technology, and bioengineering, gene therapy has been applied in patients with LSDs. As one of the vectors of gene therapy, adeno-associated virus (AAV) has good prospects in the treatment of genetic and metabolic diseases. More and more studies have shown that AAV-mediated gene therapy is effective in LSDs. This article reviews the application of AAV-mediated gene therapy in LSDs.

Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/ß-Catenin Signaling Pathway.

Allicin, an organic sulfur compound extracted from the bulb of Allium sativum, can potentially prevent various tumors. Our previous study found that allicin can effectively suppress the proliferation of osteosarcoma cells. However, the molecular mechanisms have not been illustrated. In this study, Saos-2 and U2OS osteosarcoma cells were used to investigate the underlying mechanisms. A series of experiments were carried out to authenticate the anticancer property of allicin. Knockdown of lncRNA MALAT1 inhibited the proliferation, invasion and migration and promoted apoptosis of osteosarcoma cells. Knockdown of miR-376a increased the proliferation, invasion, and migration and dropped apoptosis of osteosarcoma cells. Furthermore, knockdown of miR-376a reversed the influences of MALAT1 silencing in osteosarcoma cells. Based on our data, MALAT1 could downregulate the expression of miR-376a, subsequently accelerating osteosarcoma. Moreover, oxidative stress and autophagy were identified as the potential key pathway of allicin. Allicin inhibited osteosarcoma growth and promoted oxidative stress and autophagy via MALATI-miR-376a. We also found that allicin promotes oxidative stress and autophagy to inhibit osteosarcoma growth by inhibiting the Wnt/ß-catenin pathway in vivo and in vitro. All data showed that allicin promotes oxidative stress and autophagy of osteosarcoma via the MALATI-miR-376a-Wnt/ß-catenin pathway.

Mangiferin, a natural glucoxilxanthone, inhibits mitochondrial dynamin-related protein 1 and relieves aberrant mitophagic proteins in mice model of Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) is the second most common neurodegenerative disease featured to mitochondrial dysfunction in neuronal cells. Dynamin-related protein 1 (Drp1) is an important regulator of mitochondrial fission and subsequent mitophagy. Mangiferin (MGF) is a glucosyl xanthone mainly derived from Mangifera indica L., possessing multifaceted properties, e.g., antioxidant, anti-inflammatory, and enhancement of cognitive ability. Besides, it can cross the blood-brain barrier, thereby exerting a neuroprotective effect. However, so far, MGF's effect in balancing mitochondrial homeostasis via regulation of Drp1 level and mitophagic pathway in PD remains rarely reported. PURPOSE: We aimed to investigate the neuroprotective effect of MGF against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD and examine the possible mechanisms. METHODS: We utilized C57BL/6 mice exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP); Behavioral parameters, containing the open field test, balance beam, pole test, and rotarod test, assessed the locomotor activity; immunohistochemistry assessed the number of TH-positive neurons; transmission electron microscopy detected ultrastructural mitochondrial morphology in the dopaminergic neuron; complex I enzymatic activity microplate assay kit measured the mitochondrial complex I activity; ATP determination kit measured ATP levels in mitochondria isolated from cells or striatal tissues; western blot measured the levels of Drp1 and mitophagic proteins. RESULTS: We observed that MGF could mitigate motor deficiency and improve the expression of tyrosine hydroxylase in the substantia nigra of MPTP-induced PD mice. Furthermore, MGF not only ameliorated mitochondrial ultrastructure, but also improved mitochondrial ATP content. Within mitochondria, MGF could reduce Drp1 expression and reverse the expressions of mitophagic proteins, including PINK1, Parkin, NIX, BNIP3, FUNDC1, and p62. CONCLUSION: Present study indicates that MGF benefits mitochondrial networks by recovering mitochondrial ultrastructure and ATP contents, reducing mitochondrial Drp1, and modulating mitophagic proteins in the MPTP-induced PD mice model, which revealed a novel acting mechanism of MGF in PD's treatment.

Poly(rC) Binding Protein 1 Represses the Translation of STAT3 through 5' UTR.

BACKGROUND: Signal transducer and activator of transcription 3 (STAT3) is an oncogene and frequently overexpressed in cancers. However, the regulatory mechanisms of STAT3 expression are not fully understood. Poly(rC)-binding protein1 (PCBP1) is an RNA-binding protein that regulates mRNA stability, splicing, and translation. PCBP1 is a tumor suppressor and can inhibit the translation of several oncogenic genes. OBJECTIVE: We aimed to understand the regulatory mechanisms of STAT3 expression. METHODS: The 5' UTR or 3' UTR regions of the human STAT3 gene were inserted upstream or downstream of the green fluorescent gene (GFP), respectively, which were used as reporter systems to analyze the inhibitory effects of PCBP1 on the STAT3 gene expression. The deletion and point mutation in 5' UTR were used to search the essential regulatory sequences of the translation inhibition. The mutations of PCBP1 protein were analyzed in the cBioPortal online service. The effects of mutated PCBP1 proteins on STAT3 expression, cancer cell proliferation, and colony formation were analyzed in oral squamous cell carcinoma (OSCC) cell lines. RESULTS: PCBP1 inhibits mRNA translation through a motif in the 5' UTR of STAT3. Moreover, we found two leucine residues (Leu100 and Leu102) of PCBP1 protein frequently mutated in cancers. These mutations abolished the inhibition function of PCBP1 on STAT3 translation. Surprisingly, in contrast to wild-type PCBP1 protein, these mutations can promote the growth and colony formation of cancer cells. CONCLUSION: Overall, we demonstrate that PCBP1 can inhibit the expression of STAT3 through its 5' UTR, and two leucine residues of PCBP1 protein are essential for its functions.

A randomized controlled trial: evaluation of efficiency and safety of a novel surgical guide in the extraction of deeply impacted supernumerary teeth in the anterior maxilla.

Background: Preoperative X-ray and cone-beam computed tomography (CBCT) are helpful for locating supernumerary teeth, but the images cannot be transferred to the operation. To design a novel surgical guide plate for intraoperative navigation, we transfer the patient's oral CBCT and gypsum model scan data to a computer for analysis. In our study, we evaluate the efficiency and safety of a novel surgical guide plate for the extraction of deeply impacted supernumerary teeth (DIMSNT) in the anterior maxilla. Methods: Forty patients treated at the Department of School & Hospital of Stomatology, Wenzhou Medical University from March 2019 to December 2020 with DIMSNT (type II/III according to Liu et al.) in the anterior maxilla were randomly divided into 2 groups (20 patients for each group) for the extraction. For group I, a novel surgical guide was selected using CBCT and gypsum model scan. In contrast, for group II who underwent freehand surgery, only the CBCT data was used. The evaluation of operation time, complications, satisfaction score, and the number of cases that underwent extraction immediately after removing the bone were performed to assess the efficiency and safety of this novel surgical plate. Results: All patients completed the surgery successfully. The guides for group I had a good application effect. Group I's operation time (23.35±5.39 min) was shorter than group II (29.60±9.76 min) (P=0.0194). The average pain degree of group I (1.8±1.08) was significantly less than group II (2.82±1.68) (P<0.05). The average swelling score of group I (34) was significantly less than group II (44.7). Patient satisfaction was significantly higher in group I (8.95±1.05) than in group II (7.90±1.51) (P=0.0152). Conclusions: The novel surgical guide assisted with DIMSNT extraction have been effective in improving the quality of the surgery, patient satisfaction, and reduce its difficulty and duration. We can construct a surgical guide plate to guide the incision and osteotomy in DIMSNT surgery through the data analysis of DIMSNT on computer, which has a broad application prospect for clinical use. Trial registration: Chinese Clinical Trial Registry ChiCTR2100054523.

P75 neurotrophin receptor positively regulates the odontogenic/osteogenic differentiation of ectomesenchymal stem cells via nuclear factor kappa-B signaling pathway.

p75NTR, a neural crest stem cell marker, is continuously expressed in mesenchymal cells during tooth development. Importantly, high expression of p75NTR in the late bell stage implicates its involvement in odontogenesis and mineralization. However, the regulatory mechanisms underlying p75NTR involvement in odonto/osteogenic differentiation remain unclear. Here, we investigate the effect and potential mechanisms underlying p75NTR involvement in odonto/osteogenic differentiation. We dissected EMSCs from the first branchial arches of mice embryo and compared the proliferation and migration of p75NTR+/+ and p75NTR-/-EMSCs by transwell, scratch and cell counting kit 8(CCK8)assays. The differentiation ability and the involvement of nuclear factor kappa-B (NF-κB) pathway were investigated through alkaline phosphatase and immunofluorescence assay, real-time PCR, and western blot. During induction of dental epithelium conditioned medium, p75NTR+/+ EMSCs exhibited deeper Alkaline phosphatase (ALP) staining and higher expression of odonto/osteogenic genes/proteins (e.g., dentin sialoprotein (DSPP) than p75NTR+/+ EMSCs. Moreover, p75NTR+/+ EMSCs exhibited higher nuclear P65 expression than p75NTR-/-EMSCs. Inhibition of NF-κB pathway with Bay11-7082 in p75NTR+/+EMSCs substantially decreased DSPP expression level. However, activation of NF-κB pathway with Bay11-7082 in p75NTR-/-EMSCs enhanced DSPP expression level. Thus, p75NTR possibly plays a paramount role in the proliferation and differentiation of EMSCs via NF-κB pathway.

Efficacy and safety of istradefylline for Parkinson's disease: A systematic review and meta-analysis.

As an adenosine receptor A2A antagonist, istradefylline is used as an adjunctive agent of levodopa to improve motor symptoms in advanced Parkinson's disease (PD) patients. In this study, we re-evaluated the effects of istradefylline on treating the motor symptoms of PD patients. We performed a literature search up to November 2021 from electronic databases. Eligible studies were synthesized for efficacy, tolerability, OFF time, Unified Parkinson's Disease Rating Scale part III score, ON state with dyskinesia, and the incidence of treatment-emergent adverse events. As a result, nine clinical studies with 2727 subjects on istradefylline treatment for PD patients were included. Our results showed that compared to placebo, istradefylline exhibited a statically significant difference in efficacy (1.39 [1.15 to 1.69]; p = 0.001), decreasing OFF time (-0.58 [-1.01 to - 0.16]; p = 0.007), and improving ON state with dyskinesia (0.69 [0.02 to 1.37]; p = 0.043). For tolerability, UPDRS III, and adverse effects, there was no significant difference between istradefylline and placebo. In conclusion, the results suggest that istradefylline exhibits an efficient and well-tolerated role in treating PD patients. Randomized controlled trials and long-term studies are still required to investigate the effects of istradefylline on motor and non-motor symptoms of PD in future research.

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway.

OBJECTIVE: Qiyusanlong (QYSL) formula has been used in the clinic for more than 20 years and has been proved to have pronounced efficacy in the treatment of non-small-cell lung cancer (NSCLC). This work aims to evaluate the molecular mechanism of QYSL formula action on NSCLC, specifically in relation to autophagy induction. METHODS: In vitro, CCK-8 was used to detect the effect of QYSL serum on cell viability in A549 cells. In vivo, A549 cells were implanted subcutaneously in nude mice to establish a xenograft model. TUNEL staining was used to measure cell apoptosis and TEM to observe the autophagy-related morphological changes in vitro and in vivo. Western blotting, RT-qPCR, and immunofluorescence were used to measure autophagy-related proteins. In addition, rapamycin (an inhibitor of mTOR and inducer of autophagy) and MHY1485 (an activator of mTOR and inhibitor of autophagy) were used to determine whether QYSL-induced autophagy was regulated by the mTOR pathway. RESULTS: QYSL serum inhibited the cell viability of A549 cells in a concentration-dependent manner. In vivo, the QYSL formula inhibited xenograft growth. The QYSL formula promoted apoptosis in A549 cells and induced autophagosome formation in vitro and in vivo. In addition, the QYSL formula downregulated the expression of mTOR and p62, while it upregulated the expression of ATG-7 and Beclin-1 and increased the LC3-II/LC3-I ratio. QYSL serum inhibited p-mTOR in a similar manner to rapamycin while reducing the activating effects of MHY1485 on p-mTOR. CONCLUSION: The QYSL formula has anti-lung cancer effects and promotes autophagy through the mTOR signaling pathway.

Effects of medial meniscal slope and medial posterior tibial slope on the locations of meniscal tears: A retrospective observational study.

The aim of this study was to analyze the relationship between medial posterior tibial slope (MPTS) and medial meniscus slope (MMS) with the location of meniscal lesions. We hypothesize that meniscuses with greater MPTS and MMS are more likely to have lesions in posterior horn.A total of 292 patients underwent arthroscopic surgery between January 2014 to September 2019 due to knee osteoarthritis (OA) and meniscal lesions were reviewed. Based upon the location of meniscal tears, patients were categorized as group B (tears in posterior horn) and group A (other sites). MPTS and MMS were measured from magnetic resonance imaging (MRI) slices. Osteoarthritis grade was evaluated in anteroposterior radiographs by the criteria defined by Kellgeren and Lawrence. Demographic data, OA grade, MPTS, and MMS for the 2 groups were compared and analyzed.The group A had 29 (39%) male and 45 (61%) female subjects with a mean age of 57.07 ±â€Š6.79 years. Group B consists of 74 (34%) male and 144 (66%) female subjects with a mean age of 58.90 ±â€Š7.594 years. (P = .067 and P = .458 for age and sex, respectively). In group A, 31 knees (42%) were determined to be Kellgren-Lawrence grade one, 32 knees (43%) grade two, and 11 knees (15%) grade three. In group B, 86 knees (39%) were categorized in grade one, 85 knees (39%) in grade two, and 47 knees (26%) in grade three (P = .085). The mean MPTS was 5.06 ±â€Š2.11 degree for group A and 6.15 ±â€Š2.37 degree for group B (P = .001). The mean MMS for group A was lower than group B (1.38 ±â€Š2.12 degree vs 3.14 ±â€Š2.92 degree; P < .000)This study demonstrated that increased MPTS and MMS may be considered as the risk factors for medial meniscal posterior horn tears.

LncRNA OR3A4 Regulated the Growth of Osteosarcoma Cells by Modulating the miR-1207-5p/G6PD Signaling.

BACKGROUND: Increasing evidence has demonstrated the importance of non-coding RNAs including long non-coding RNA (lncRNA) and microRNAs (miRNAs) in the tumorigenesis of osteosarcoma (OS). Abnormal expression of lncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) was found in multiple human cancers; however, the function of OR3A4 in OS remains largely unknown. MATERIALS AND METHODS: The expression level of OR3A4 in OS tissues and cell lines was detected by RT-qPCR. Cell counting kit-8 assay, colony formation and flow cytometry analysis were performed to determine the growth of OS cells. The targets of OR3A4 were predicted using the miRDB database. The binding between OR3A4 and miRNAs was confirmed by dual-luciferase reporter assay. RESULTS: OR3A4 was overexpressed in OS tissues and correlated with the advanced progression of OS patients. Down-regulation of OR3A4 significantly inhibited the proliferation and colony formation of OS cells. Mechanistically, OR3A4 acted as a sponge of miR-1207-5p. Glucose-6-phosphate dehydrogenase (G6PD) was identified as a target of miR-1207-5p. Knockdown of OR3A4 increased the expression of miR-1207-5p and consequently, suppressed the level of G6PD in OS cells. Due to the essential role of G6PD in the pentose phosphate pathway (PPP), depletion of OR3A4 inhibited NADPH production, glucose consumption and lactate generation. Decreased level of NADPH by depletion of OR3A4 up-regulated the redox state (ROS) content and resulted in endoplasmic reticulum (ER) stress in OS cells. Restoration of G6PD significantly attenuated the cell growth inhibition induced by OR3A4 knockdown. CONCLUSION: Our finding suggested the critical role of OR3A4 in the proliferation of OS cells via targeting the miR-1207-5p/G6PD axis.

Underexpression of SRSF3 and its target gene RBMX predicts good prognosis in patients with head and neck cancer.

Head and neck cancer collectively is one of the most common cancer types in the world. Oral squamous cell carcinoma (OSCC) is the most common subtype of head and neck cancer. SRSF3 is a proto-oncogene and is overexpressed in patients with OSCC. However, the relationship between SRSF3 expression and the clinical outcomes of patients with head and neck cancer remains unclear. By using the cBioPortal for Cancer Genomics, a public online tool originally developed at Memorial Sloan Kettering Cancer Center (New York, NY, USA), it was revealed that patients with head and neck cancer with an underexpression of SRSF3 showed better overall and disease-/progression-free survival rates. Moreover, 227 genes were found to be significantly coexpressed with SRSF3 in head and neck cancer. Then, in combination with the analysis of a previous splice-array dataset that included significantly changed genes after the silencing of SRSF3, four potential target genes of SRSF3 were identified. RBMX and HNRNPL were further confirmed to be target genes of SRSF3. Moreover, the underexpression of RBMX was determined to be significantly associated with a favorable overall survival rate among patients, while patients with an underexpression of both SRSF3 and RBMX is a subgroup of individuals with better prognoses than all other patients. These results suggest that the underexpression of SRSF3 and that of its target RBMX can be used as potential biomarkers to predict favorable overall survival among head and neck cancer patients.

Second-look arthroscopic findings after medial open-wedge high tibial osteotomy combined with all-inside repair of medial meniscus posterior root tears.

PURPOSE: To examine the results of medial open-wedge high tibial osteotomy (MOWHTO) combined with all-inside repair focusing on medial meniscus posterior root tears (MMPRT) by second-look arthroscopy and determine the clinical relevance of the findings. METHODS: From June 2015 to June 2017, 27 consecutive patients underwent MOWHTO and meniscal treatment for MMPRT using all-inside repair. All were available for second-look arthroscopy evaluation at the time of plate removal. Cartilage regeneration in the medial condyles and healing status of the MMPRT were assessed at the time of second-look arthroscopy. Clinical outcomes were evaluated by the Hospital for Special Surgery (HSS) scores and the Lysholm score scale. The potential factors affecting the healing of MMPRT, including age, body mass index (BMI), weight-bearing line rate (WBLR) and femorotibial angle (FTA) were discussed. RESULTS: There were 11 (41%) cases with complete healing (group A) and 16 (59%) cases with lax healing (group B). A complete cartilage coverage of chondral lesions was observed at second-look arthroscopy. Improvements of HSS in both groups were 41.25 ± 6.18 and 38.82 ± 5.43, while improvements in Lysholm score seen in both groups were 30.40 ± 4.84 and 32.65 ± 4.11. There was no significant difference in the postoperative clinical results between the two groups. In group A, the age (months), BMI, WBLR, and FTA are 54.61 ± 2.53, 23.58 ± 2.39, 66.10 ± 2.86% and 169.00 ± 2.62°, respectively, while in group B, they are 55.16 ± 4.92, 29.58 ± 3.91, 57.51 ± 5.49% and 175.21 ± 2.87°, respectively. A significant difference has been identified between two groups except for age. CONCLUSION: As seen in this retrospective study, a higher healing rate of MMPRT using all-inside repair and regeneration of degenerated articular cartilage in the medial condyles after MOWHTO can be expected. Healing of the MMPRT was not related to a better clinical outcome. Moreover, it can be inferred that BMI, WBLR and FTA may affect the healing status of MMPRT.