Preeclampsia is a placenta-originated disorder closely associated with impaired placental development and immune imbalance at the maternal-fetal interface. As a critical process in the regulation of cellular homeostasis, autophagy plays a pivotal role in trophoblast syncytialization, invasion, and immune tolerance at the maternal-fetal interface. Moderate autophagy enhances trophoblast function and promotes spiral artery remodeling, whereas insufficient or excessive autophagy correlates with placental pathological features of preeclampsia, including impaired syncytialization, protein aggregate accumulation, and immune dysregulation. Although trophoblast-specific autophagy deficiencies in animal models can manifest preeclampsia-like phenotypes, clinical studies reveal tissue-specific variability in autophagy-related protein expression, which may be attributable to placental regional heterogeneity, disease subtypes, and sampling timepoints. Future investigations integrating multi-stage clinical cohorts, multicellular models, and genetically modified animals are warranted to elucidate the dynamic role of autophagy in preeclampsia pathogenesis and establish its causal relationship with disease progression, thereby providing a basis for targeted therapeutic strategies.

Laparoscopic technology has become an important choice for ventral hernia repair due to its advantages of minimal trauma and rapid recovery. Traditional non-absorbable synthetic meshes are the most commonly used type of mesh in laparoscopic ventral hernia repair. Although they provide reliable mechanical support, their long-term presence in the human body may cause mesh erosion and wrinkling, leading to complications such as intestinal fistula, abdominal adhesions, postoperative foreign body sensation, chronic pain, and infection, which are receiving increasing attention. Absorbable meshes, with their excellent biocompatibility and ability to induce tissue remodelling, can reduce the incidence of the above complications and are revolutionising laparoscopic ventral hernia repair. The authors introduce the types and characteristics of existing absorbable mesh, focusing on their clinical efficacy in laparoscopic ventral hernia repair, existing challenges and countermeasures, as well as individualized surgical decision-making in laparoscopic ventral hernia repair.

Laparoscopic technology has become an important choice for ventral hernia repair due to its advantages of minimal trauma and rapid recovery. Traditional non-absorbable synthetic meshes are the most commonly used type of mesh in laparoscopic ventral hernia repair. Although they provide reliable mechanical support, their long-term presence in the human body may cause mesh erosion and wrinkling, leading to complications such as intestinal fistula, abdominal adhesions, postoperative foreign body sensation, chronic pain, and infection, which are receiving increasing attention. Absorbable meshes, with their excellent biocompatibility and ability to induce tissue remodelling, can reduce the incidence of the above complications and are revolutionising laparoscopic ventral hernia repair. The authors introduce the types and characteristics of existing absorbable mesh, focusing on their clinical efficacy in laparoscopic ventral hernia repair, existing challenges and countermeasures, as well as individualized surgical decision-making in laparoscopic ventral hernia repair.

Preeclampsia is a placenta-originated disorder closely associated with impaired placental development and immune imbalance at the maternal-fetal interface. As a critical process in the regulation of cellular homeostasis, autophagy plays a pivotal role in trophoblast syncytialization, invasion, and immune tolerance at the maternal-fetal interface. Moderate autophagy enhances trophoblast function and promotes spiral artery remodeling, whereas insufficient or excessive autophagy correlates with placental pathological features of preeclampsia, including impaired syncytialization, protein aggregate accumulation, and immune dysregulation. Although trophoblast-specific autophagy deficiencies in animal models can manifest preeclampsia-like phenotypes, clinical studies reveal tissue-specific variability in autophagy-related protein expression, which may be attributable to placental regional heterogeneity, disease subtypes, and sampling timepoints. Future investigations integrating multi-stage clinical cohorts, multicellular models, and genetically modified animals are warranted to elucidate the dynamic role of autophagy in preeclampsia pathogenesis and establish its causal relationship with disease progression, thereby providing a basis for targeted therapeutic strategies.

Obesity has emerged as a significant public health concern with profound implications for human well-being. Bariatric metabolic surgery can significantly reduce the weight of patients with severe obesity and improve the related complications, and has been widely used in clinical practice. With the growth of surgical amount, the occurrence of postoperative hypoglycemia, in addition to surgery-related adverse events, has gradually attracted clinical attention. Post-bariatric hypoglycemia (PBH) occurs 6-12 months after bariatric metabolic surgery. It is characterized by blood glucose levels ≤2.8~3.3 mmol/L within 1-3 hours after a meal, accompanied by symptoms of sympathetic nervous system activation and even neuroglycopenic symptoms. Limited epidemiological investigations suggest that the prevalence of PBH ranges from 0.2% to 44.2%. Notably, severe and recurrent hypoglycemic events have deleterious implications for patients, significantly compromising their quality of life and posing a potential threat to their life safety. Consequently, the management of PBH warrants comprehensive clinical attention.

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