肠道炎症性疾患(Inflammatory Bowel Disease)是一种慢性全身性炎症疾病,主要包括溃疡性结肠炎(Ulcerative Colitis, UC)以及克罗恩病(Crohn’s Disease, CD)特征是肠道黏膜受到广泛的炎症破坏。此外,其可涉及全身各个系统,形成系统性合并症,骨骼系统便是其中之一。肠道炎症患者或各式各样的动物模型中均可观察到骨质破坏以及骨量丧失的现象,而这其中的病因机制却涉及各个方面,包括营养状况、炎症因子、肠道激素类信号分子以及肠道菌群等。总的来说骨代谢的平衡主要依赖于成骨与破骨作用之间的平衡,外界或内部因素倘若打破这一平衡,便会引起宏观方面的骨骼系统的变化,肠道炎症状态下亦是如此。本文将从肠道炎症状态出发,对这一病理环境下骨代谢异常的表现以及病因机制以及相关治疗策略做一综述。Inflammatory Bowel Disease, as a chronic systemic inflammatory disease that includes Ulcerative Colitis (UC) and Crohn’s disease (CD), is characterized by extensive inflammatory destruction of the intestinal mucosa. In addition, it involves various systems throughout the body, leading to systemic comorbidities, especially the skeletal system. Bone destruction and bone loss have been observed in patients with intestinal inflammation or in various animal models, and the etiological mechanism of this phenomenon involves various aspects, including nutritional status, inflammatory factors, intestinal hormone signaling molecules, and intestinal flora. In general, the balance of bone metabolism mainly depends on the balance between osteogenesis and osteoclastogenesis. If external or internal factors break this balance, it would cause changes in the skeletal system in the macro aspect, and this is also the case in the state of intestinal inflammation. Starting from the state of intestinal inflammation, this article will review the manifestations, etiological mechanisms and related treatment strategies of abnorma
糖尿病(Diabetes Mellitus, DM)是全球高发的代谢性疾病,严重影响患者的生活质量并导致了一系列并发症。糖酵解作为细胞主要的能量生产途径之一,与DM及其并发症的发生和发展密切相关。近年来,糖酵解在DM中的研究取得了重要进展,研究表明糖酵解途径中关键酶的异常表达可能是DM及其并发症的核心病理机制之一。糖酵解的异常不仅破坏了能量代谢的平衡,还可能通过毒性代谢产物的积累加剧糖尿病肾病(DN)、糖尿病心肌病(DCM)、糖尿病视网膜病变(DR)、糖尿病神经病变(DPN)、糖尿病脑血管病(DCVD)等并发症的进展。靶向糖酵解关键酶的治疗策略,展现出对DM及其并发症治疗的巨大潜力,并为新的治疗方法提供了理论依据。Diabetes mellitus (DM) is a globally prevalent metabolic disorder that significantly affects patients’ quality of life and leads to various complications. As one of the primary energy-producing pathways in cells, glycolysis is closely associated with the onset and progression of DM and its complications. In recent years, substantial progress has been made in understanding the role of glycolysis in DM. Studies have demonstrated that abnormal expression of key enzymes in the glycolytic pathway may be a fundamental pathological mechanism underlying DM and its complications. Dysregulated glycolysis not only disrupts energy metabolism homeostasis but also contributes to the accumulation of toxic metabolic byproducts, thereby exacerbating diabetic nephropathy (DN), diabetic cardiomyopathy (DCM), diabetic retinopathy (DR), diabetic peripheral neuropathy (DPN), and diabetic cerebrovascular disease (DCVD). Therapeutic strategies targeting key glycolytic enzymes have shown great potential in the treatment of DM and its complications, providing a theoretical basis for novel therapeutic approaches.
