Ferroptosis is an iron-driven cell death modality characterized by iron accumulation and excessive lipid peroxidation. Ferroptosis is closely related to mitochondrial function, as indicated by studies showing that mitochondrial dysfunction and damage promote oxidative stress, which in turn induces ferroptosis. Mitochondria play crucial roles in cellular homeostasis, and abnormalities in their morphology and function are closely associated with the development of many diseases. Mitochondria are highly dynamic organelles, and their stability is maintained through a series of regulatory pathways. Mitochondrial homeostasis is dynamically regulated, mainly via key processes such as mitochondrial fission, mitochondrial fusion and mitophagy; however, mitochondrial processes are prone to dysregulation. Mitochondrial fission and fusion and mitophagy are intimately related to ferroptosis. Therefore, investigations into the dynamic regulation of mitochondrial processes during ferroptosis are important to provide a better understanding of the development of disease. In this paper, we systematically summarized changes in ferroptosis, mitochondrial fission and fusion and mitophagy to promote an in-depth understanding of the mechanism underlying ferroptosis and provide a corresponding reference for the treatment of related diseases.

The N(6)-methyladenosine (m6A) modification is the most pervasive modification of human RNAs. In recent years, an increasing number of studies have suggested that m6A likely plays important roles in cancers. Many studies have demonstrated that m6A is involved in the biological functions of cancer cells, such as proliferation, invasion, metastasis, and drug resistance. In addition, m6A is closely related to the prognosis of cancer patients. In this review, we highlight recent advances in understanding the function of m6A in various cancers. We emphasize the importance of m6A to cancer progression and look forward to describe future research directions.

Acute pancreatitis (AP) is an acute inflammatory disease of the exocrine pancreas. The pathogenesis of AP is still unclear, and there is currently no specific treatment. A variety of immune cells infiltrate in AP, which may play an important role in the progression of the disease. In this study, for the first time, scRNA-Seq and Bulk RNA-Seq data were used to show the characteristics of immune cell infiltration in AP, and to explore the specific molecular markers of different cell types. The present study also investigated cell-to-cell communication networks using the CellChat package, and AP-specific gene signatures (Clic1, Sat1, Serpina3n, Atf3, Lcn2, Osmr, Ccl9, Hspb1, Anxa2, Krt8, Cd44, Cd9, Hsp90aa1, Tmsb10, Hmox1, Fxyd5, Plin2, Pnp) were identified through integrative analysis of multiple sequencing datasets. We also defined disease-specific associated genes in different cell types, revealing dynamic changes through cell trajectory and pseudo-time analysis using the Monocle2 package. The results showed that macrophages were significantly increased in acute pancreatitis, and the number of interactions and interaction weight/strength of the macrophages in AP were significantly higher than those in the controls. The activities of various signaling pathways were abnormally regulated such as apoptosis, oxidative stress, lysosome, autophagy, ferroptosis, and inflammatory responses signaling pathways. In conclusion, this study comprehensively depicted the immune microenvironment of AP, explored the interaction network between different cell types, and defined AP-specific gene signatures, providing many new directions for basic research in AP.

Primary closure following laparoscopic common bile duct exploration (LCBDE) has been widely adopted because of the efficacy and safety in treatment of common bile duct (CBD) stones. However, the risk factors for bile leakage, the most common complication after primary closure, has not been clarified yet. A retrospective cohort study of patients who underwent LCBDE with primary closure after choledochotomy between Feb. 2012 and Jun. 2016 was performed. Risk factors for bile leakage were identified by logistic regression inculding demographic factors, preoperative condition and surgical details. Between Feb. 2012 and Jun. 2016, a total of 265 LCBDE procedures were applied in our hospital and 141 patients with primary closure were included in this study. Bile leakage occurred in 11.3% (16/141) of these patients, and happened more frequently in patients with slender CBD (<1 vs ≥1 cm, 31.6% vs 7.0%, p = 0.04) and those managed by inexperienced surgeons (initial 70 cases vs later cases, 17.1% vs 5.6%, p = 0.04). After multivariable regression, the diameter of CBD [OR 95% CI, 3.799 (1.081–13.349), p = 0.04] and experience of surgeons [OR 95% CI, 4.228 (1.330–13.438), p = 0.03] were significantly related to bile leakage. Slender CBD and inexperienced surgeons were the high risk factors for bile leakage after primary closure following LCBDE.

Acute pancreatitis (AP) is an inflammatory disease that can progress to severe acute pancreatitis (SAP), which increases the risk of death. AP is characterized by inappropriate activation of trypsinogen, infiltration of inflammatory cells, and destruction of secretory cells. Other contributing factors may include calcium (Ca²⁺) overload, mitochondrial dysfunction, impaired autophagy, and endoplasmic reticulum (ER) stress. In addition, exosomes are also associated with pathophysiological processes of many human diseases and may play a biological role in AP. However, the pathogenic mechanism has not been fully elucidated and needs to be further explored to inform treatment. Recently, the treatment guidelines have changed; minimally invasive therapy is advocated more as the core multidisciplinary participation and “step-up” approach. The surgical procedures have gradually changed from open surgery to minimally invasive surgery that primarily includes percutaneous catheter drainage (PCD), endoscopy, small incision surgery, and video-assisted surgery. The current guidelines for the management of AP have been updated and revised in many aspects. The type of fluid to be used, the timing, volume, and speed of administration for fluid resuscitation has been controversial. In addition, the timing and role of nutritional support and prophylactic antibiotic therapy, as well as the timing of the surgical or endoscopic intervention, and the management of complications still have many uncertainties that could negatively impact the prognosis and patients’ quality of life. Consequently, to inform clinicians about optimal treatment, we aimed to review recent advances in the understanding of the pathogenesis of AP and its diagnosis and management.