Objective To explore the tumor shrinking pattern, the image evaluation methods of the residual lesions after neoadjuvant chemotherapy, and the indications, the resection range, the surgical margins, the management of sentinel lymph node biopsy (SLNB) and axillary lymph nodes of breast conserving surgery after neoadjuvant chemotherapy. Methods Domestic and foreign literatures about the breast conserving surgery after neoadjuvant chemotherapy were collected and reviwed. Results Breast conserving surgery after neoadjuvant chemotherapy raised the rate of breast conserving surgery and improved the postoperative life quality of patients, while the overall survival rate had no significant difference compared with mastectomy. Tumor shrinking pattern and its related factors after neoadjuvant chemotherapy remain required further study. At present, the indications for breast conserving surgery after neoadjuvant chemotherapy still mainly refered to that for early stage breast cancer. Resection range was more recognized to the scope of residual tumor lesions after chemotherapy. The margins were more widely accepted as which were without tumor involved. Although there were some controversies about the use of SLNB and the management of axillary lymph nodes based on the results of SLNB in breast conserving surgery after neoadjuvant chemotherapy, it was still considered necessary at the basis of the accurate biopsy technique acquired. Conclusions At present, breast conserving treatment after neoadjuvant chemotherapy is considered safe and effective. However, it is necessary to proceed cautiously under the conditions of adequate communication of local recurrence rate, standardized local treatment, standard postoperative radiotherapy, systemic adjuvant therapy, and regular follow-up.
Diabetic retinopathy (DR) is the most common microvascular complication in patients with diabetes and a leading cause of vision loss. Recent studies have shown that inflammation and oxidative stress play central roles in its development and progression. Hyperglycemia activates systemic immune cells and retinal resident cells, inducing the release of various inflammatory mediators and chemokines, which disrupt the blood-retinal barrier, leading to capillary leakage and neurodegenerative changes. Meanwhile, the positive feedback loop between inflammation and reactive oxygen species/nitric oxide further amplifies pathological damage, explaining the limited efficacy of anti-vascular endothelial growth factor monotherapy. Oxidative stress manifests as the excessive generation of free radicals such as reactive oxygen species due to hyperglycemia, directly damaging retinal cells and activating inflammatory signaling pathways, thereby exacerbating vascular damage and neurodegeneration. Future therapeutic strategies should adopt multi-target and multi-link interventions, with particular emphasis on the combined application of anti-inflammatory and antioxidant treatments, such as immunomodulation, macrophage phenotype regulation, intervention in the neutrophil extracellular trap axis, and combination therapy using anti-vascular endothelial growth factor drugs and antioxidants, to more effectively intervene in the pathological progression of DR.