Zhonghua wei zhong bing ji jiu yi xue最新文献

Sepsis-associated acute kidney injury (SAKI) is a life-threatening complication of sepsis, whose pathogenesis involves the intricate interplay of multiple factors, including dysregulated host immune-inflammatory responses, microcirculatory disturbances, and metabolic dysfunction. Aberrations in epigenetic modifications, including DNA methylation and histone acetylation, dynamically modulate gene expression networks, thereby influencing cellular metabolic reprogramming, activation of pro-inflammatory signaling pathways, and disruption of microvascular barrier integrity, are closely associated with adverse clinical outcomes in SAKI patients. As a central regulatory hub of gene expression, epigenetic modifications profoundly participate in key pathological processes of SAKI, including immune homeostasis imbalance, metabolic dysregulation, and microcirculatory dysfunction, through remodeling chromatin architecture and non-coding RNA expression profiles. Although emerging evidence suggests that targeting epigenetic regulation may mitigate SAKI-related pathological damage, the precise molecular mechanisms remain incompletely elucidated. This review systematically summarizes the regulatory roles and molecular mechanisms of epigenetic modifications in SAKI, aiming to provide a theoretical foundation for advancing the understanding of SAKI pathogenesis and developing novel therapeutic strategies.

Extracorporeal membrane oxygenation (ECMO) is primarily used in clinical practice to provide continuous extracorporeal respiratory and circulatory support for patients with severe heart and lung failure, thereby sustaining life. It is a key technology for managing severe heart failure and respiratory failure that are difficult to control. With the accumulation of clinical experience in ECMO for circulatory and/or respiratory support, as well as advancements in biomedical engineering technology, more portable and stable ECMO devices have been introduced into clinical use, benefiting an increasing number of critically ill patients. Although ECMO technology has become relatively mature, the timing of ECMO initiation, management of sudden complications, and monitoring and early warning of physiological indicators are critical factors that greatly affect the therapeutic outcomes of ECMO. This article reviews traditional methods and artificial intelligence techniques used in risk assessment related to ECMO, including the latest achievements and research hotspots. Additionally, it discusses future trends in ECMO risk management, focusing on six key areas: multi-center and prospective studies, external validation and standardization of model performance, long-term prognosis considerations, integration of innovative technologies, enhancing model interpretability, and economic cost-effectiveness analysis. This provides a reference for future researchers to build models and explore new research directions.

Traumatic brain injury (TBI), as a significant central nervous system damage disease with high frequency in the world, leads to a huge number of patients with impaired health and lower quality of life every year. Lung injury is a common and dangerous consequence, which dramatically raises the mortality of patients. Discovering the pathophysiology of lung injury after TBI and discovering viable therapeutic targets has become an important need for clinical diagnosis and therapy. Neurotransmitters, as the fundamental chemical agents of the nervous system for signal transmission, not only govern neuronal activity and apoptosis in TBI but also significantly influence the pathophysiological mechanisms of lung injury subsequent to TBI. The imbalance is intricately linked to the onset and progression of lung damage. This paper systematically reviews the clinical characteristics and predominant pathogenesis of lung injury following TBI, emphasizing the role of key neurotransmitters, including glutamate (Glu), γ-aminobutyric acid (GABA), norepinephrine (NE), dopamine (DA), and acetylcholine (ACh), in lung injury post-TBI. It examines their influence on inflammatory response, vascular permeability, and pulmonary circulation function. Additionally, the paper evaluates the research advancements and potential applications of targeted therapeutic strategies for various neurotransmitter systems, such as receptor antagonists, transporter inhibitors, and neurotransmitter analogues. This research aims to offer a theoretical framework for clarifying the neural regulatory mechanisms of lung injury following TBI and to establish a basis for the development of novel therapeutic strategies and enhancement of the prognosis of the patients.