Delayed wound healing causes problems for many patients both physically and psychologically, contributing to pain, economic burden, loss of function, and even amputation. Although many factors affect the wound healing process, abnormally prolonged or augmented inflammation in the wound site is a common cause of poor wound healing. Excessive neutrophil extracellular trap (NET) formation during this phase may amplify inflammation and hinder wound healing. However, the roles of NETs in wound healing are still unclear. Herein, we briefly introduce NET formation and discuss the possible NET-related mechanisms in wound healing. We conclude with a discussion of current studies, focusing on the roles of NETs in diabetic and normoglycemic wounds and the effectiveness of NET-targeting treatments in wound healing.

Renal ischemia‒reperfusion injury (IRI) is one of the main causes of acute kidney injury (AKI), which is a potentially life-threatening condition with a high mortality rate. IRI is a complex process involving multiple underlying mechanisms and pathways of cell injury and dysfunction. Additionally, various types of cell death have been linked to IRI, including necroptosis, apoptosis, pyroptosis, and ferroptosis. These processes operate differently and to varying degrees in different patients, but each plays a role in the various pathological conditions of AKI. Advances in understanding the underlying pathophysiology will lead to the development of new therapeutic approaches that hold promise for improving outcomes for patients with AKI. This review provides an overview of the recent research on the molecular mechanisms and pathways underlying IRI-AKI, with a focus on regulated cell death (RCD) forms such as necroptosis, pyroptosis, and ferroptosis. Overall, targeting RCD shows promise as a potential approach to treating IRI-AKI.

Neutrophil extracellular traps (NETs) are involved in the activation and dysfunction of multiple overlapping and interacting pathways, including the immune response to injury, inflammation, and coagulation, which contribute to the pathogenesis of sepsis-induced acute lung injury (SI-ALI). However, how NETs mediate the relationship between inflammation and coagulation has not been fully clarified. Here, we found that NETs, through stimulator of interferon genes (STING) activation, induced endothelial cell damage with abundant production of tissue factor (TF), which magnified the dysregulation between inflammatory and coagulant responses and resulted in poor prognosis of SI-ALI model mice. Disruption of NETs and inhibition of STING improved the outcomes of septic mice and reduced the inflammatory response and coagulation. Furthermore, Toll-like receptor 2 (TLR2) on the surface of endothelial cells was involved in the interaction between NETs and the STING pathway. Collectively, these findings demonstrate that NETs activate the coagulant cascade in endothelial cells in a STING-dependent manner in the development of SI-ALI.

Acute kidney injury (AKI) is a common and serious complication of cardiac surgery and is associated with increased mortality and morbidity, accompanied by a substantial economic burden. The pathogenesis of cardiac surgery-associated acute kidney injury (CSA-AKI) is multifactorial and complex, with a variety of pathophysiological theories. In addition to the existing diagnostic criteria, the exploration and validation of biomarkers is the focus of research in the field of CSA-AKI diagnosis. Prevention remains the key to the management of CSA-AKI, and common strategies include maintenance of renal perfusion, individualized blood pressure targets, balanced fluid management, goal-directed oxygen delivery, and avoidance of nephrotoxins. This article reviews the pathogenesis, definition and diagnosis, and pharmacological and nonpharmacological prevention strategies of AKI in cardiac surgical patients.

Purpose: This study aimed to evaluate effects of remote ischemic preconditioning (RIPC) on myocardial injury in patients undergoing off-pump coronary artery bypass graft surgery (OPCABG). Methods: Sixty-five patients scheduled for the OPCABG were randomly assigned to control (n = 32) or RIPC group (n = 33). All patients received general anesthesia. Before the surgical incision, RIPC was induced on an upper limb with repeated 5-min ischemia and 5-min reperfusion for four times. Blood samples were collected from right internal jugular vein. Plasma levels of IL-6, IL-8, IL-10, TNF-α, cTnT, HFABP, IMA, and MDA were detected at pre-operatively and 0, 6, 18, 24, 48, 72, and 120 h after the surgery. Left internal mammary artery (LIMA) and great saphenous vein (GSV) was cut into 2–3 mm for Western blot analysis of Hif-1α. Results: In the present study, RIPC treatment significantly reduced plasma levels of cardiac troponin T (p < 0.05), heart-type fatty acid binding protein (p < 0.05), ischemia modified albumin (p < 0.05), malondialdehyde (p < 0.05), as well as plasma levels of pro-inflammatory cytokines including IL-6, IL-8, and TNF-α (P < 0.05, respectively). RIPC treatment significantly increased hypoxia-inducible factor-1α (p < 0.05) expression as well. Mechanical ventilation time for postoperative patients was shortened in RIPC group than those in control group (17.4 ± 3.8 h vs. 19.7 ± 2.9 h, respectively, p < 0.05). Conclusion: RIPC by upper limb ischemia shortens mechanical ventilation time in patients undergoing OPCABG. RIPC treatment reduces postoperative myocardial enzyme expression and pro-inflammatory cytokine production. RIPC is a protective therapeutic approach in the coronary artery bypass graft surgery.

Background: Minimally invasive cardiac surgery (MICS) is increasingly performed due to faster recovery time and lower postoperative complications when compared with the traditional open surgery. However, hypoxemia in lung isolation duration after cardiopulmonary bypass (CPB) surgery has been the focus of anesthesiologists’ attention. In the present study, we designed a novel lung isolation strategy to improve oxygenation using a bronchial blocker (BB) to isolate the right middle and lower lobes and preserve the ventilated right upper lobe without affecting the surgical field. Methods: Patients who had undergone right lateral mini-thoracotomy, a MICS, between August 2018 and February 2019, were enrolled in this randomized controlled study. Patients were randomly divided into a modified lung isolation group (group M) and a conventional lung isolation group (group C). In group M, BBs were used to block the bronchus intermedius, while left-sided double lumen endotracheal tubes were used in group C to isolate the right lung. The primary outcome was to determine the number of patients who required an increase in ventilation volume due to hypoxemia during lung isolation after CPB. Results: Sixty-one patients (30 in group C and 31 in group M) were enrolled. Five patients in group M were converted to right lung isolation due to poor surgical field exposure. During lung isolation after CPB, the number of patients with hypoxemia was lower in group M than group C (5/31 vs. 15/30, P=0.005). Conclusions: The novel modified lung isolation strategy reduced the incidence of hypoxemia after CPB.