a-teleoperated-robotic-system-assisted-percutaneous-transiliac

A Teleoperated Robotic System-Assisted Percutaneous Transiliac-Transsacral Screw Fixation Technique

Transiliac-transsacral screw fixation is challenging in clinical practice as the screws need to break through six layers of cortical bone. ...

treatment-with-locking-intramedullary-nailing-for-intertrochanteric

Treatment with Locking Intramedullary Nailing for Intertrochanteric Fracture of the Femur Utilizing a New Awl with a Distal Positioner

Interlocked intramedullary nailing is now established as the preferred method of managing femoral intertrochanteric fractures. Choosing the ideal entry ...

Huazhong University of Science and Technology

Huazhong University of Science & Technology

The transiliac-transsacral screw placement is a clinical challenge for surgeons. This study explored a point-to-point coaxial guide apparatus assisting the transiliac-transsacral screw insertion and aimed to investigate the feasibility and accuracy of the guide apparatus in the treatment of posterior ring unstable pelvic fracture compared with a free-hand technique.

A useful intraoperative technique for transiliac-transsacral screws: a point-to-point coaxial guide apparatus.

Hemophilic arthropathy (HA) is a typically iron overload induced joint disease secondary to continuous joint bleeding, however, the exact role of iron chelators in HA has not been fully elucidated. In the present study, we investigated whether desferoxamine (DFO), an iron chelator, could limit the development of HA and the underlying mechanisms.

Desferoxamine protects against hemophilic arthropathy through the upregulation of HIF-1α-BNIP3 mediated mitophagy.

Osteoarthritis (OA) is a multifactorial and increasingly prevalent degenerative disease that affects the whole joint. The pathogenesis of OA is poorly understood and there is a lack of therapeutic interventions to reverse the pathological process of this disease. Accumulating studies have shown that the overproduction of reactive oxygen species (ROS) and ROS-induced lipid peroxidation are involved in the pathogenesis of OA. 4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) have received considerable attention for their role in cartilage degeneration and subchondral bone remodeling during OA development. Ferroptosis is a form of cell death characterized by a lack of control of membrane lipid peroxidation and recent studies have suggested that chondrocyte ferroptosis contributes to OA progression. In this review, we aim to discuss lipid peroxidation-derived 4-HNE and MDA in the progression of OA. In addition, the therapeutic potential for OA by controlling the accumulation of lipid peroxidation and inhibiting chondrocyte ferroptosis are discussed.

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis.

Osteoarthritis (OA) is a prevalent degenerative disease of the elderly. The NRF2 antioxidant system plays a critical role in maintaining redox balance. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant. This research aimed to determine whether MitoQ alleviated OA and the role of the NRF2/Parkin axis in MitoQ-mediated protective effects. In interleukin (IL)-1β-induced OA chondrocytes, MitoQ activated the NRF2 pathway, reducing extracellular matrix (ECM) degradation and inflammation. MitoQ also increased glutathione peroxidase 4 (GPX4) expression, leading to decreased levels of reactive oxygen species (ROS) and lipid ROS. Silencing NRF2 weakened MitoQ's protective effects, while knockdown of Parkin upregulated the NRF2 pathway, inhibiting OA progression. Intra-articular injection of MitoQ mitigated cartilage destruction in destabilized medial meniscus (DMM)-induced OA mice. Our study demonstrates that MitoQ maintains cartilage homeostasis  and  through the NRF2/Parkin axis. We supplemented the negative feedback regulation mechanism between NRF2 and Parkin. These findings highlight the therapeutic potential of MitoQ for OA treatment.

Mitoquinone alleviates osteoarthritis progress by activating the NRF2-Parkin axis.

Ferroptosis is involved in the pathogenesis of osteoarthritis (OA) while suppression of chondrocyte ferroptosis has a beneficial effect on OA. However, the molecular mechanism of ferroptosis in OA remains to be elucidated. P21, an indicator of aging, has been reported to inhibit ferroptosis, but the relationship between P21 and ferroptosis in OA remains unclear. Here, we aimed to investigate the expression and function of P21 in OA chondrocytes, and the involvement of P21 in the regulation of ferroptosis in chondrocytes. First, we demonstrated that high P21 expression was observed in the cartilage from OA patients and destabilized medial meniscus (DMM) mice, and in osteoarthritic chondrocytes induced by IL-1β, FAC and erastin. P21 knockdown exacerbated the reduction of Col2a1 and promoted the upregulation of MMP13 in osteoarthritic chondrocytes. Meanwhile, P21 knockdown exacerbated cartilage degradation in DMM-induced OA mouse models and decreased GPX4 expression in vivo. Furthermore, P21 knockdown sensitized chondrocytes to ferroptosis induced by erastin, which was closely associated with the accumulation of lipid peroxides. In mechanism, we demonstrated that P21 regulated the stability of GPX4 protein, and the regulation was independent of NRF2. Meanwhile, we found that P21 significantly affected the recruitment of GPX4 to linear ubiquitin chain assembly complex (LUBAC) and regulated the level of M1-linked ubiquitination of GPX4. Overall, our results suggest that P21 plays an essential anti-ferroptosis role in OA by regulating the stability of GPX4.

P21 resists ferroptosis in osteoarthritic chondrocytes by regulating GPX4 protein stability.

Excess iron contributes to Hemophilic Arthropathy (HA) development. Divalent metal transporter 1 (DMT1) delivers iron into the cytoplasm, thus regulating iron homeostasis.

DMT1-mediated iron overload accelerates cartilage degeneration in Hemophilic Arthropathy through the mtDNA-cGAS-STING axis.

Osteoarthritis (OA) is the most common chronic pathema of human joints. The pathogenesis is complex, involving physiological and mechanical factors. In previous studies, we found that ferroptosis is intimately related to OA, while the role of Sat1 in chondrocyte ferroptosis and OA, as well as the underlying mechanism, remains unclear.

Inhibition of SAT1 alleviates chondrocyte inflammation and ferroptosis by repressing ALOX15 expression and activating the Nrf2 pathway.

Z-DNA binding protein 1 (ZBP1) is a nucleic acid sensor that is involved in multiple inflammatory diseases, but whether and how it contributes to osteoarthritis (OA) are unclear.

IRF1 regulation of ZBP1 links mitochondrial DNA and chondrocyte damage in osteoarthritis.

Osteoarthritis (OA) is a significant contributor to disability in the elderly population. However, current therapeutic options are limited. The transient receptor potential melastatin 2 (TRPM2) is involved in a range of disease processes, yet its role in OA remains unclear.

TRPM2-mediated feed-forward loop promotes chondrocyte damage in osteoarthritis via calcium-cGAS-STING-NF-κB pathway.

The most common joint disease in the elderly is osteoarthritis (OA), which is characterized by synovitis, cartilage degeneration, and osteophytes, for which there are currently no effective therapies. Chondrocytes, responsible for extracellular matrix (ECM) synthesis and degradation, undergo changes in OA, leading to ECM disruption and disease progression. There is no clear role for the Mechanistic target of rapamycin complex 2 (mTORC2) in OA, but it is known to regulate cellular functions, such as proliferation, metabolism, motility, and apoptosis. The purpose of this study was to determine the molecular mechanism by which Rapamycin-insensitive companion of mTOR (RICTOR), a component of mTORC2, contributes to OA progression. The results demonstrate that IL-1β induces high expression of RICTOR in chondrocytes, promoting downregulation of collagen II expression and impairing autophagy. Silencing RICTOR reverses IL-1β-induced downregulating of collagen II expression and mitochondrial dysfunction. RICTOR inhibits chondrocyte autophagy by inhibiting autophagosome formation and preventing autophagosome-lysosome fusion. Additionally, RICTOR promotes oxidative stress in chondrocytes, leading to disruption of normal mitochondrial structure and disturbance of the articular cartilage microenvironment. This study reveals the potential of RICTOR to treat OA. Specifically, blocking mTORC2 might be an effective treatment strategy.

RICTOR-mediated activation of AKT/mTOR signaling and autophagy inhibition promote osteoarthritis.

Osteosarcoma (OS), the most prevalent primary malignant bone tumor in children and adolescents, arises from bone-forming mesenchymal cells. Despite advancements in surgical resection and neoadjuvant chemotherapy (cisplatin, doxorubicin, and methotrexate), chemotherapy resistance remains a significant challenge, leading to poor survival rates in patients with metastatic or recurrent OS.

OTULIN confers cisplatin resistance in osteosarcoma by mediating GPX4 protein homeostasis to evade the mitochondrial apoptotic pathway.

Iron homeostasis is critical for multiple physiological and pathological processes. DMT1, a core iron transporter, is expressed in almost all cells and organs and altered in response to various conditions, whereas, there is few reviews focusing on DMT1 in diseases associated with aberrant iron metabolism. Based on available knowledge, this review described a full view of DMT1 and summarized the roles of DMT1 and DMT1-mediated iron metabolism in the onset and development of inflammatory and degenerative diseases. This review also provided an overview of DMT1-related treatment in these disorders, highlighting its therapeutic potential in chronic inflammatory and degenerative diseases.

The Roles of DMT1 in Inflammatory and Degenerative Diseases.

Paraptosis is a novel form of programmed cell death, generally caused by disrupted proteostasis or alterations of redox homeostasis. However, its impact and underlying mechanisms on the pathology of osteoarthritis (OA) are still unclear. This study aimed to investigate the role and regulatory mechanism of SHP2 in chondrocyte paraptosis and the effects influenced by low-intensity pulsed ultrasound (LIPUS).

ArticleTotal : 2	Year
Publication title Cited by 2	2023
Publication title	2025

Article	Year
A useful intraoperative technique for transiliac-transsacral screws: a point-to-point coaxial guide apparatus. Journal of orthopaedic surgery and research\| PubMed ID: 33509244	2021
Desferoxamine protects against hemophilic arthropathy through the upregulation of HIF-1α-BNIP3 mediated mitophagy. Life sciences\| PubMed ID: 36410411	2023
Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis. Cell death discovery\| PubMed ID: 37644030	2023
Mitoquinone alleviates osteoarthritis progress by activating the NRF2-Parkin axis. iScience\| PubMed ID: 37694150	2023
P21 resists ferroptosis in osteoarthritic chondrocytes by regulating GPX4 protein stability. Free radical biology & medicine\| PubMed ID: 38176476	2024
DMT1-mediated iron overload accelerates cartilage degeneration in Hemophilic Arthropathy through the mtDNA-cGAS-STING axis. Biochimica et biophysica acta. Molecular basis of disease\| PubMed ID: 38331112	2024
Inhibition of SAT1 alleviates chondrocyte inflammation and ferroptosis by repressing ALOX15 expression and activating the Nrf2 pathway. Bone & joint research\| PubMed ID: 38447596	2024
IRF1 regulation of ZBP1 links mitochondrial DNA and chondrocyte damage in osteoarthritis. Cell communication and signaling : CCS\| PubMed ID: 39026271	2024
TRPM2-mediated feed-forward loop promotes chondrocyte damage in osteoarthritis via calcium-cGAS-STING-NF-κB pathway. Journal of advanced research\| PubMed ID: 39505144	2024
RICTOR-mediated activation of AKT/mTOR signaling and autophagy inhibition promote osteoarthritis. International immunopharmacology\| PubMed ID: 39591826	2025
OTULIN confers cisplatin resistance in osteosarcoma by mediating GPX4 protein homeostasis to evade the mitochondrial apoptotic pathway. Journal of experimental & clinical cancer research : CR\| PubMed ID: 39721999	2024
The Roles of DMT1 in Inflammatory and Degenerative Diseases. Molecular neurobiology\| PubMed ID: 39775481	2025
SHP2-mediated ROS activation induces chondrocyte paraptosis in osteoarthritis and is attenuated by low-intensity pulsed ultrasound. Journal of orthopaedic translation\| PubMed ID: 40337549	2025

Zehang Zheng

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