Objective: This study aimed to investigate the nurse-patient trust among in-patients in the context of the COVID-19 epidemic; it further analyzed the related influencing factors, which will provide a theoretical basis for developing corresponding measures. Methods: This study employed a mixed-method design and analyzed 149 patients at the Hongqi Hospital, affiliated with Mudanjiang Medical University, from December 2020 to February 2021. Quantitative analysis was carried out using the “Nurse Patient Trust Scale,” and qualitative analysis was performed using a semi-structured interview with in-patients. Results: The average score on the scale was 46.65 ±2.83, and the scores of the two dimensions were: 23.24 ±1.51 for ability and peace of mind, and 23.32 ±1.53 for attitude and care. According to the interview data, the factors included three aspects: a comfortable hospital environment and humane management measures; the nurse’s own competence; effective communication with patients. Conclusion: During the COVID-19 epidemic, there are still many factors affecting patients’ trust in nurses that can be addressed by taking different measures. All these factors must be considered by the relevant managers and clinical nursing staff to maintain a better nurse-patient trust relationship.

Wound healing may be disrupted by lipopolysaccharide (LPS)‐induced mitochondrial dysfunction, inflammation, and excessive oxidative stress, which can lead to undesirable consequences. The haematopoietic cell‐specific protein 1‐associated protein X‐1 (HAX‐1) is a mitochondrial matrix protein that regulates mitochondrial function. This study aimed to comprehensively identify the role of HAX‐1 in the inhibition of LPS‐induced mitochondrial dysfunction and apoptosis in human dermal fibroblasts (HDFs). HAX‐1 expression was assessed in the HDF‐a cell line using real‐time polymerase chain reaction, western blotting, and immunohistochemical staining. The viability, migration, and apoptosis of HDF‐a cells were evaluated using the water‐soluble tetrazolium‐1 assay, transwell assay, and flow cytometry analysis, respectively. Mitochondrial function was evaluated based on reactive oxygen species (ROS) generation and mitochondrial membrane potential (ΔΨm). Our results demonstrated that LPS stimulation markedly repressed HAX‐1 expression in HDFs and silencing of HAX‐1 led to mitochondrial ROS accumulation, ΔΨm disruption, and abnormal mitochondrial morphology. Accordingly, overexpression of HAX‐1 or administration of metformin enhanced mitochondrial fusion and normalized mitochondrial dynamics, thereby reversing LPS‐induced mitochondrial dysfunction, fibroblast apoptosis, and viability and migration inhibition in HDF‐a cells. These data support a mechanism wherein HAX‐1 plays a crucial role in LPS‐induced fibroblast apoptosis in a mitochondria‐dependent manner.