Acute mesenteric ischemia (AMI) defines a complex of conditions characterized by an interruption of the splanchnic circulation, leading to insufficient oxygen delivery or utilization to fill the metabolic needs of the visceral organs. Early diagnosis and immediate therapy are the cornerstones of early ischemia to reach a successful outcome and are necessary to reduce the high mortality. Although there is still lack of specific biomarkers to assist the diagnosis of AMI in clinical practice, there are several biomarkers with high specificity, may become a potential tools in early diagnosis of AMI, including intestinal fatty acid binding protein (I-FABP), a-glutathione S-transferase (a-GST), D-dimer, L-and D-lactate, citrulline, ischemia modified albumin, procalcitonin (PCT). However, they use in clinical limited duo to the many studies about these makers finished with small patient populations, and heterogeneous among these populations. This review describes the etiology of AMI, the current most studied promising biomarkers, the current research situation and future of biomarker research.

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Purpose Chemically induced acute lung injury (CALI) has become a serious health concern in our industrialized world, and abnormal functional alterations of immune cells crucially contribute to severe clinical symptoms. However, the cell heterogeneity and functional phenotypes of respiratory immune characteristics related to CALI remain unclear. Methods We performed scRNA sequencing on bronchoalveolar lavage fluid (BALF) samples obtained from phosgene-induced CALI rat models and healthy controls. Transcriptional data and TotalSeq technology were used to confirm cell surface markers identifying immune cells in BALF. The landscape of immune cells could elucidate the metabolic remodeling mechanism involved in the progression of acute respiratory distress syndrome and cytokine storms. We used pseudotime inference to build macrophage trajectories and the corresponding model gene expression changes, and identified and characterized alveolar cells and immune subsets that may contribute to CALI pathophysiology based on gene expression profiles at single-cell resolution. Results The immune environment of cells, including dendritic cells and specific macrophage subclusters, exhibited increased function during the early stage of pulmonary tissue damage. Nine different subpopulations were identified that perform multiple functional roles, including immune responses, pulmonary tissue repair, cellular metabolic cycle, and cholesterol metabolism. Additionally, we found that individual macrophage subpopulations dominate the cell-cell communication landscape. Moreover, pseudo-time trajectory analysis suggested that proliferating macrophage clusters exerted multiple functional roles. Conclusion Our findings demonstrate that the bronchoalveolar immune microenvironment is a fundamental aspect of the immune response dynamics involved in the pathogenesis and recovery of CALI.