Pingjin Zou’s research while affiliated with University of Electronic Science and Technology of China and other places

Background Poly (ADP-ribose) polymerase inhibitors (PARPi) serve as crucial therapeutic agents in solid tumor treatment. Preclinical investigations suggest a potential protective function of PARPi against endocrine and metabolic impairments. Nevertheless, the existing body of evidence remains inconclusive on this aspect. Purpose Our aim was to evaluate the potential impact of PARPi on endocrine and metabolic disruptions in clinical trials. Data sources We conducted a comprehensive search across the Medline, EMBASE, PubMed, and Web of Science databases, along with the ClinicalTrials.gov registry. Study selection Phase II/III randomized controlled trials (RCTs) investigating the effects of PARPi in metabolic and endocrine processes were selected for inclusion in patients with solid tumors. Data extraction The primary outcomes of interest encompassed metabolic and endocrine dysfunctions. Data synthesis A total of 26 trials (n = 9,590 patients) were included in our meta-analysis. Niraparib demonstrated an increased risk of any-grade hyperglycemia (OR = 2.15, 95% CI 1.28–3.62), with patients receiving PARPi for metastatic pancreatic cancer showing a higher susceptibility to any-grade hyperglycemia (OR = 1.78, 95% CI 1.04–3.04). Conversely, rucaparib exhibited a potential ameliorative effect on hyperglycemia (OR = 0.54, 95% CI 0.30–0.97). No statistically significant disparities were observed for other outcomes associated with PARPi utilization. Limitations Among these RCTs included, 50% were assessed as low qualities due to high risk of bias. Conclusions Our meta-analysis demonstrated that PARPi may exert adverse effects on endocrine and metabolic pathways. Close monitoring of hyperglycemia is recommended for patients undergoing niraparib therapy, especially those with pancreatic cancer. Trial registration This meta-Analysis was prospectively registered in the PROSPERO database with ID CRD42023457959. Graphical Abstract

Purpose Radiation-induced pulmonary fibrosis (RIPF) is a serious complication of radiotherapy that lacks effective treatment options. The Huaxian formula (HXF), a traditional Chinese herbal remedy, shows promise in alleviating RIPF; however, its active ingredients and underlying mechanisms remain poorly understood. Methods Through serum pharmacochemistry, network pharmacology, molecular docking, and experimental validation, we investigate the potential mechanisms of HXF in the prevention and treatment of radiation-induced pulmonary fibrosis (RIPF). Results Histological examination and non-invasive computed tomography (CT) scans in animal experiments revealed that HXF improved extracellular matrix collagen deposition in the lung tissue of irradiated mice and reduced fibrosis manifestations on CT images. Analysis of post-HXF administration serum samples identified 21 enriched compounds as potential active compounds, with 430 corresponding prospective targets. Overlapping these compounds with 991 RIPF-related genes yielded 127 genes primarily associated with the PI3K-Akt signaling pathway, EGFR tyrosine kinase inhibitor resistance, and the MAPK signaling pathway. Molecular docking indicated that key compounds in HXF serum, 5,7,8-trimethoxyflavone, and hyperoside, exhibited strong affinity with key targets. Finally, animal experiments confirmed that HXF significantly inhibited the expression of p-Akt and p-PI3K proteins in the lung tissue of irradiated mice. Conclusion Our research results indicate that HXF may exert its effects on the prevention and treatment of radiation-induced pulmonary fibrosis (RIPF) through multiple pathways and targets, with the PI3K-Akt signaling pathway likely playing the most crucial role in this process.

Esophageal cancer is the eighth most common cancer worldwide and the sixth leading cause of cancer-related deaths. In this study, we propose a novel esophageal stent equipped with a wireless, battery-free, and movable photodynamic therapy (PDT) unit designed to treat esophageal tumors with flexibility, precision, and real-time control. This system integrates a PDT unit and an electrochemical pneumatic soft actuator into a conventional esophageal stent. Each module incorporates a piezoelectric transducer capable of receiving external ultrasound to power the respective module. These transducers selectively respond to different external ultrasound frequencies, enabling independent operation without mutual interference. The therapy module provides a light source for PDT, inducing the production of cytotoxic reactive oxygen species (ROS) in tumor cells and promoting apoptosis. The pneumatic actuator based on electrochemical principles plays a critical role in controlling the position of the PDT light source, enabling the movement of the therapy module up to 200 mm within 15 min. This allows real-time control to maintain the light source near the tumor, ensuring precise and targeted treatment. The system can wirelessly and in real-time control the PDT light source's position via external ultrasound, offering a novel approach for treating esophageal cancer patients according to the need of tumor's progression.

Photodynamic therapy (PDT) represents a targeted approach for cancer treatment that employs light and photosensitizers (PSs) to induce the generation of reactive oxygen species (ROS). However, PDT faces obstacles including insufficient PS localization, limited light penetration, and treatment resistance. A potential solution lies in nanogenerators (NGs), which function as self-powered systems capable of generating electrical energy. Recent progress in piezoelectric and triboelectric NGs showcases promising applications in cancer research and drug delivery. Integration of NGs with PDT holds the promise of enhancing treatment efficacy by ensuring sustained PS illumination, enabling direct electrical control of cancer cells, and facilitating improved drug administration. This comprehensive review aims to augment our comprehension of PDT principles, explore associated challenges, and underscore the transformative capacity of NGs in conjunction with PDT. By harnessing NG technology alongside PDT, significant advancement in cancer treatment can be realized. Herein, we present the principal findings and conclusions of this study, offering valuable insights into the integration of NGs to overcome barriers in PDT.

Wearable and implantable triboelectric nanogenerators (TENGs) convert mechanical energy to electricity in the daily movements of the human body. Self-generated dynamic electric field or displacement current of TENGs can operate from micrometers to centimeters, which offers a key technology for TENG-based therapy systems for precision medicine on both tissues and cells. TENGs have low-current and high-voltage properties, which reduce damage to normal tissues, and kill rapidly dividing cancer cells. In this work, the dynamic electric field from TENG directly inhibits the cellular proliferation behavior of cancer cells. The work paves a new way for the self-generated electric field of TENG for cancer therapy.

Wearable and implantable triboelectric nanogenerators (TENGs) convert mechanical energy to electricity in the daily movements of the human body. Self‐generated dynamic electric field or displacement current of TENGs can operate from micrometers to centimeters, which offers a key technology for TENG‐based therapy systems for precision medicine on both tissues and cells. TENGs have low‐current and high‐voltage properties, which reduce damage to normal tissues, and kill rapidly dividing cancer cells. In this work, the dynamic electric field from TENG directly inhibits the cellular proliferation behavior of cancer cells. The work paves a new way for the self‐generated electric field of TENG for cancer therapy.

The effective and targeted treatment of resistant cancer cells presents a significant challenge. Targeting cell ferroptosis has shown remarkable efficacy against apoptosis‐resistant tumors due to their elevated iron metabolism and oxidative stress levels. However, various obstacles have limited its effectiveness. To overcome these challenges and enhance ferroptosis in cancer cells, we have developed a self‐powered photodynamic therapeutic tablet that integrates a ferroptosis inducer (FIN), imidazole ketone erastin (IKE). FINs augment the sensitivity of photodynamic therapy (PDT) by increasing oxidative stress and lipid peroxidation. Furthermore, they utilize the Fenton reaction to supplement oxygen, generating a greater amount of reactive oxygen species (ROS) during PDT. Additionally, PDT facilitates the release of iron ions from the labile iron pool (LIP), accelerating lipid peroxidation and inducing ferroptosis. In vitro and in vivo experiments have demonstrated a more than 85% tumor inhibition rate. This synergistic treatment approach not only addresses the limitations of inadequate penetration and tumor hypoxia associated with PDT but also reduces the required medication dosage. Its high efficiency and specificity towards targeted cells minimize adverse effects, presenting a novel approach to combat clinical resistance in cancer treatment.