Intervertebral disc degeneration (IVDD) refers to the aging and degenerative diseases of intervertebral disc components such as nucleus pulposus, annulus fibrosus, and cartilage endplate, and is the main cause of chronic low back pain. Over the past few years, many researchers around the world concerned that the degeneration of nucleus pulposus (NP) cells plays the main role in IVDD. The degeneration of NP cells is caused by a series of pathological processes, including oxidative stress, inflammatory response, apoptosis, abnormal proliferation, and autophagy. Interestingly, many studies have found a close relationship between the senescence of NP cells and the progression of NP degeneration. The classical aging pathways also have been confirmed to be involved in the pathological process of IVDD. Moreover, several anti-aging drugs have been used to treat IVDD by inhibiting NP cells senescence, such as proanthocyanidins, resveratrol and bone morphogenetic protein 2. Therefore, this article will systematically list and discuss aging, cell senescence, the pathogenesis and targeted therapies of IVDD, in order to provide new ideas for the treatment of IVDD in the future.

Platelets are blood cells that are primarily produced by the shedding of megakaryocytes in the bone marrow. Platelets participate in a variety of physiological and pathological processesin vivo, including hemostasis, thrombosis, immune-inflammation, tumor progression, and metastasis. Platelets have been widely used for targeted drug delivery therapies for treating various inflammatory and tumor-related diseases. Compared to other drug-loaded treatments, drug-loaded platelets have better targeting, superior biocompatibility, and lower immunogenicity. Drug-loaded platelet therapies include platelet membrane coating, platelet engineering, and biomimetic platelets. Recent studies have indicated that platelet extracellular vesicles (PEVs) may have more advantages compared with traditional drug-loaded platelets. PEVs are the most abundant vesicles in the blood and exhibit many of the functional characteristics of platelets. Notably, PEVs have excellent biological efficacy, which facilitates the therapeutic benefits of targeted drug delivery. This article provides a summary of platelet and PEVs biology and discusses their relationships with diseases. In addition, we describe the preparation, drug-loaded methods, and specific advantages of platelets and PEVs targeted drug delivery therapies for treating inflammation and tumors. We summarize the hot spots analysis of scientific articles on PEVs and provide a research trend, which aims to give a unique insight into the development of PEVs research focus.

Osteoarthritis (OA) is a progressive degenerative disorder which severely threatens the quality of life of older individuals. OA progression is closely related to heightened levels of mitochondrial reactive oxygen species (mtROS). Although nanozymes have a good ROS-scavenging effect, they cannot precisely scavenge mtROS because of the immune rejection of cell membranes, lysosomal escape, and the inability of conventional nanozymes to directly target mitochondria. Dual-target nanozymes were engineered to precisely scavenge mtROS in chondrocytes. We used chondrocyte membrane-camouflaged TPP-modified hollow Prussian blue nanozymes and subsequently encapsulated these nanozymes in a hybrid glycyrrhizic acid hydrogel. The therapeutic efficacy and underlying mechanisms were assessed in vitro and in vivo. The novel nanozymes enhanced cell selectivity, immune evasion capabilities, and mitochondrial targeting. The dual-targeted nanozymes exerted a pronounced therapeutic impact on inflammatory chondrocytes, mitigated mtDNA leakage by precisely scavenging mtROS, dampened cGAS-STING-NF-κB signaling, and enhanced chondrocyte function. The hybrid hydrogels also exhibited improved therapeutic outcomes. We confirmed the beneficial effects of the nanozyme-hydrogel combination on OA progression in mice. The nanozyme-hydrogel combination can reduce precisely scavenge mtROS in chondrocytes, avoiding the leakage of mtDNA and suppressing the cGAS-STING-NF-κB signaling pathway, thereby decreasing inflammatory responses and alleviate OA progression.

Objective: To assess the clinical efficacy and share the technique notes of Wiltse Approach TLIF for the treating single segment degenerative lumbar spinal disease.Method: In this retrospective controlled study, 780 patients with single segment degenerative lumbar disease who were operated in our hospital from January 2016 to December 2020 were analyzed retrospectively. The patients were randomly assigned to Wiltse approach group (group A, 410 cases) and conventional open approach group (group B, 370 cases). Patient's assessment of pain and disability were evaluated by the visual analogue scale (VAS) and the Oswestry disability index (ODI) before and after surgery. The incision length, operative time, exposure time, intraoperative blood loss, hidden blood loss, time to ambulation, total length of hospitalization, serum creatine kinase, X‐rays, CT and MRI were also evaluated.Results: There were no differences in sex, age, pre‐operative ODI score, VAS score between the two groups (P > 0.05). The Wiltse approach group had a shorter incision length with 7.69 ± 0.44 cm compared to the conventional group with 11.13 ± 0.36 cm (P < 0.01). The average operative time was 119.20 ± 14.64 min with exposure time of 16.20 ± 3.42 min in the Wiltse approach group and 145.65 ± 16.98 min with 29.20 ± 3.42 min in the conventional group (P < 0.05, P < 0.01). Comparing the intraoperative blood loss, hidden blood loss, serum creatine kinase, time to ambulation, total length of hospitalization, the Wiltse approach group was less than the conventional open approach group (P < 0.05). The VAS score of the two groups decreased significantly with time, and the VAS score of the Wiltse group was significantly lower than that of the conventional open approach group (P < 0.05). At last investigation after operation, ODI scores of the two groups were significantly decreased compared with that before operation. Wiltse approach group was significantly lower than that of the conventional open approach group (P < 0.05). The multifidus of the two groups of patients had a certain degree of atrophy. But the Wiltse approach group multifidus muscle atrophy rate is significantly lower than the conventional open approach group.Conclusion: The Wiltse approach TLIF significantly reduces the damage to the paravertebral muscles and the postoperative incidence of chronic low back pain.

Background: This study aimed to reveal the associations of osteoporotic vertebral compression refracture (OVCRF) incidence with sarcopenia and paravertebral muscles (PVM). Methods: A total of 214 elderly patients who underwent percutaneous kyphoplasty in our hospital between January 2017 and December 2019 were analyzed. Data on possible risk factors, including sex, age, weight, height, diabetes, treated vertebral levels (thoracolumbar junction [(T10–L2]), vacuum clefts, and body mass index (BMI), were collected. Preoperative bone mineral density (BMD) and appendicular muscle mass were evaluated using dual-energy X-ray absorptiometry. Nutritional status was evaluated using the Mini Nutritional Assessment. Magnetic resonance imaging was performed to evaluate the physiological cross-sectional area of the PVM. Results: Overall, 74 (15 men and 59 women) and 60 (55 women and 14 men) patients developed OVCRF and sarcopenia, respectively. Sarcopenia is related to advanced age, ower BMD and BMI values. Sarcopenia-related indicators (PVM fat rate, appendicular muscle mass index, grip strength) were significantly lower in the sarcopenia group. Univariate analysis showed a correlation between OVCRF and BMD, BMI, diabetes, sarcopenia, and age. Multivariate analysis suggested that fatty infiltration of the PVM, BMD, sarcopenia, diabetes, BMI, and treated vertebral level remained as the independent predictors of OVCRF (p < 0.05). Conclusions: The association between sarcopenia and PVM as independent risk factors for OVCRF was established in this study; therefore, sarcopenia should be greatly considered in OVCRF prevention.

In humans, the trachea is a conduit for ventilation connecting the throat and lungs. However, certain congenital or acquired diseases may cause long-term tracheal defects that require replacement. Tissue engineering is considered a promising method to reconstruct long-segment tracheal lesions and restore the structure and function of the trachea. Decellularization technology retains the natural structure of the trachea, has good biocompatibility and mechanical properties, and is currently a hotspot in tissue engineering studies. This article lists various recent representative protocols for the generation of decellularized tracheal scaffolds (DTSs), as well as their validity and limitations. Based on the advancements in decellularization methods, we discussed the impact and importance of mechanical properties, revascularization, recellularization, and biocompatibility in the production and implantation of DTS. This review provides a basis for future research on DTS and its application in clinical therapy.