Mitochondrion: A bridge linking aging and degenerative diseases.

Aging is a natural process, characterized by progressive loss of physiological integrity, impaired function, and increased vulnerability to death. For centuries, people have been trying hard to understand the process of aging and find effective ways to delay it. However, limited breakthroughs have been made in anti-aging area. Since the hallmarks of aging were summarized in 2013, increasing studies focus on the role of mitochondrial dysfunction in aging and aging-related degenerative diseases, such as neurodegenerative diseases, osteoarthritis, metabolic diseases, and cardiovascular diseases. Accumulating evidence indicates that restoring mitochondrial function and biogenesis exerts beneficial effects in extending lifespan and promoting healthy aging. In this paper, we provide an overview of mitochondrial changes during aging and summarize the advanced studies in mitochondrial therapies for the treatment of degenerative diseases. Current challenges and future perspectives are proposed to provide novel and promising directions for future research.

A rare and highly malignant Stwart-Treves syndrome case after breast cancer surgery: a case report.

Background: Stewart-Treves syndrome (STS) is a lymphatic sarcoma secondary to chronic lymphedema of the extremities. Most STS patients have a history of breast cancer and have undergone radical mastectomy and postoperative radiation and chemotherapy. It usually occurs 11 to 12 years after surgery, and about 0.45% of patients are estimated to have the disease. The characteristics of STS include that it is clinically relatively rare, has a high degree of malignancy, can spread easily in the absence of timely treatment, and has low survival rate. Herein, we report a case of STS which developed 13 years after breast cancer-related lymphoedema (BCRL). It allows doctors to recognize and detect the disease earlier. Case Description: A 74-year-old woman had undergone modified radical mastectomy 13 years ago for invasive ductal breast cancer in her left breast. After multiple rounds of postoperative chemoradiotherapy, multiple purple lesions were found in the left upper limb during physical examination in April 2021. The lesions spread rapidly and were varied in size. An immediate skin biopsy reported the lesions as STS. The patient was diagnosed with lymphangiosarcoma with metastasis (STS). The surgical method was shoulder joint amputation, chest wall resection, and local flap transfer. After surgery, the patient underwent 6 rounds of paclitaxel 300 mg + carboplatin 300 mg chemotherapy. After chemotherapy, the patient's wound healed and the suspected metastasis disappeared. At the time of writing, she has survived for more than 13 months, and her quality of life has improved significantly, to the satisfaction of the patient and her family. The patient is able to eat normally and lead a normal life with some assistance, without significant weight loss. Conclusions: Although rare, STS is a serious invasive complication of breast cancer surgery. To increase their relative survival time, patients with BCRL need to identify and thoroughly investigate rapidly progressing skin lesions, and undergo timely surgery.

LncRNA XIST Prevents Tendon Adhesion and Promotes Tendon Repair Through the miR-26a-5p/COX2 Pathway.

Tendon adhesion is the biggest obstacle to repair of tendon injury. Long-chain non-coding RNA X-inactive specific transcript (lncRNA XIST) is highly expressed in populations at high risk of tendon injury. However, whether XIST participates in tendon injury and the specific mechanism remain unknown. Here, we aimed to explore the effects and underlying mechanism of XIST in tendon injury. A mouse model of tendon injury was constructed by the transection method in vivo. XIST and COX2 were highly expressed in tendon tissues of mice with tendon injury, while miR-26a-5p was lowly expressed. Fibroblasts were isolated from tendon injury mice. Overexpression of XIST promoted fibroblast proliferation and upregulated α-SMA and Collagen I protein expression, while silencing XIST indicated the opposite effects. Further dual-luciferase reporter gene assay and RIP assay verified a targeting relationship between XIST and miR-26a-5p, as well as miR-26a-5p and COX2, and XIST targeted miR-26a-5p to act on COX2 expression. miR-26a-5p inhibition and COX2 overexpression reversed the decrease in fibroblast proliferation and the downregulation of α-SMA and Collagen I expression caused by XIST silencing, while interference with si-COX2 eliminated the effects of miR-26a-5p inhibitor. This study revealed that XIST promoted fibroblast proliferation and the formation of tendon adhesion through miR-26a-5p/COX2 pathway, suggesting that XIST/miR-26a-5p/COX2 may be a potential target for the treatment of tendon injury.

Lycium barbarum polysaccharides exert an antioxidative effect on rat chondrocytes by activating the nuclear factor (erythroid-derived 2)-like 2 signaling pathway.

INTRODUCTION: Oxidative stress is the main cause of osteoarthritis (OA). Lycium barbarum polysaccharides (LBP) have antioxidant properties. Thus, the potential effect of LBP on H2O2-stimulated chondrocytes was examined. MATERIAL AND METHODS: The cell viability was detected by CCK-8. The reactive oxygen species (ROS) production and apoptosis rates were determined by flow cytometric analysis. The DNA damage was detected by comet assay. Real-time polymerase chain reaction (qPCR) and Western blot assays were performed to examine the expression of histone 2A family member X (γH2AX), checkpoint kinase 1 (Chk1), poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase (caspase)-3/8/9, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and its antioxidant-response element (ARE) dependent factors including heme oxygenase-1 (HO-1) and quinine oxidoreductase-1 (NQO-1). RESULTS: Compared to the H2O2 group, LBP inhibited the ROS production and DNA damage caused by H2O2 (p < 0.05), respectively. LBP inhibited the mRNA and protein expressions of γH2AX and Chk1 (p < 0.05). Meanwhile, LBP significantly decreased apoptosis (p < 0.05). And LBP inhibited the expression levels of PARP and Caspase-3/8/9 (p < 0.05). Moreover, LBP increased the expression of Nrf2, HO-1and NQO-1 (p < 0.05). Furthermore, the depletion of Nrf2 that mediated by RNA interference reversed the apoptosis and DNA damage inhibition effect of LBP (p < 0.05). CONCLUSIONS: LBP protected chondrocytes through inhibiting DNA damage and apoptosis caused by H2O2, in which the Nrf2/ARE signaling pathway played a positive role. It provided an inspiration for clinical application - developing LBP as a therapeutic agent and Nrf2 as a promising candidate.

Aucubin suppresses Titanium particles­mediated apoptosis of MC3T3­E1 cells and facilitates osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway.

Aucubin represents an iridoid glucoside separated from multiple Chinese herbs, which has been demonstrated to possess numerous pharmacological activities. In the present study, the aim was to investigate the roles and mechanisms of aucubin in the suppression of mouse MC3T3­E1 osteoblast apoptosis induced by Titanium particles and the promotion of bone formation. MTT assay and flow cytometry were performed to analyze cell viability and apoptosis, respectively. ELISA and para­nitrophenyl phosphate colorimetry were carried out to evaluate the oxidative stress markers and alkaline phosphatase (ALP). Western blotting and reverse transcription­quantitative polymerase chain reaction assays were used to evaluate the associated mRNA and protein expression. The results revealed that aucubin enhanced the cell activity of MC3T3­E1 cells treated with Ti particles. Aucubin suppressed the apoptosis of Ti particles­induced MC3T3­E1 cells and facilitated osteogenesis by affecting the B­cell lymphoma­2 (Bcl­2), Bcl­2 associated X protein, ALP and associated osteogenic factors expression. Aucubin reduced the oxidative stress in Ti particles­induced MC3T3­E1 cells. In addition, aucubin upregulated the bone morphogenetic protein 2 (BMP2)/Smads/runt related transcription factor 2 (RunX2) pathway in Ti particles­induced MC3T3­E1 cells. In conclusion, the present study confirmed that aucubin suppressed the Ti particles­mediated apoptosis of MC3T3­E1 cells and facilitated osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway.

Oncoplastic breast reconstruction with omental flap: A retrospective study and systematic review.

The increasing frequency of early breast cancer cases has driven an increasing number of patients to choose immediate reconstruction with an autologous flap. Omentum-flap-based breast reconstruction is a unique strategy that is highly suitable for repairing moderate tissue defects. However, all available evidence comes from individual reports with small numbers of cases, and the overall effectiveness and safety of the procedure have yet to be reported. Here, we reported 7 cases of laparoscopically harvested omental free flap breast reconstruction and performed a systematic review to assess the applicability and safety of this approach. The data were gathered from MEDLINE, Ovid, Google Scholar and the China Knowledge Resource Integrated Database. In total, we combined 15 articles (410 cases) for analysis. The data revealed that almost all patients (87.6%) were reported to have undergone laparoscopy instead of laparotomy; pedicle flaps were used in 90.9% of the cases, while only 5 (37 cases) used free flaps for reconstruction; and 96.6% (396/410) of all reconstruction procedures were immediate. Almost all of these cases had a small tumour burden (T0/Tis/T1 59.8%; T2 36.8%), and the distribution of tumour location was similar among the four quadrants. The cosmetic outcomes were desirable in most cases (83.9%). There were 41 complications identified in the dataset: partial graft necrosis accounted for the largest percentage (41.5%) of all events, followed by skin necrosis (19.5%), haematoma (12.2%) and wound infection (9.8%). During the follow-up period, which had a short median duration, 2 cases of tumour recurrence were reported. Overall, our systematic review found that omentum-flap-based breast reconstruction could achieve a satisfactory aesthetic outcome, especially for small breasts and tissue replacement after breast-conserving surgery, and the safety of the procedure was also acceptable.

Parthenolide inhibits hydrogen peroxide­induced osteoblast apoptosis.

Parthenolide is a natural product from the shoots of Tanacetum parthenium that has been demonstrated to have immunomodulatory effects in a number of diseases. The present study aimed to determine the effect and mechanism of parthenolide on the apoptotic ability of H2O2­induced osteoblasts. Cell viability was analyzed with a MTT assay and the apoptotic rate was subsequently measured using flow cytometry. The activity of the antioxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX), and the serum marker enzymes alkaline phosphatase (ALP), malondialdehyde (MDA) and lactate dehydrogenase (LDH) was measured. Reverse transcription­quantitative polymerase chain reaction and western blot analyses were performed to analyze the expression levels of osteogenesis and oxidative stress­associated genes. The results indicated that parthenolide increased cell viability and inhibited the apoptosis of H2O2­induced osteoblasts. Parthenolide decreased the levels of reactive oxygen species, MDA, LDH and ALP. SOD and GPX levels were increased by parthenolide in H2O2­induced osteoblasts. This suggested that parthenolide may break the equilibrium state of oxidative stress and inhibit cellular apoptosis. Parthenolide additionally increased the expression levels of oxidative stress­associated genes, including nuclear factor erythroid 2 like 2, hemeoxygenase­1 and quinone oxidoreductase 1 in H2O2­induced osteoblasts. Furthermore, parthenolide increased the expression of osteogenesis­associated genes, including runt­related transcription factor 2, osteopontin, osteocalcin and collagen 1 in H2O2­inducedosteoblasts. Therefore, it was concluded that parthenolide may be used in the treatment of osteoporosis.

Laparoscopy-assisted Chimeric Peritoneal-deep Inferior Epigastric Perforator Flap for Reconstruction of Hand and Foot.

Management of hand and foot defects with exposed tendons is a big challenge for plastic surgeons. Thin vascularized tissue offers an ideal surface for tendon excursion. OBJECTIVE: This study examines the reconstructive benefits of a laparoscopy-assisted chimeric peritoneal-deep inferior epigastric artery perforator (DIEP) flap in the treatment of hand and foot injury defects. MATERIALS AND METHODS: A retrospective review was performed on 8 patients (6 men, 2 women) that received hand or foot reconstruction with laparoscopy-assisted chimeric peritoneal-DIEP flap. Soft tissue defects of the hand or foot ranged from 16 cm x 10 cm to 22 cm x 14 cm. The peritoneum supplied by the peritoneal branches of the deep inferior epigastric artery was retrieved by laparoscopy to cover exposed extensor tendons, while the DIEP flap consisted of the cutaneous component part of this chimeric flap. RESULTS: The flaps survived in 7 of 8 patients. Partial necrosis of the chimeric flap was observed in 1 patient due to venous thrombosis. A split-thickness skin graft then was performed to achieve wound closure on that patient. Motor and sensory functions of these 8 patients improved gradually within the first-year follow-up. CONCLUSIONS: The laparoscopy-assisted chimeric peritoneal-DIEP flap is useful for reconstructing defects of the hand and foot with exposed tendons.