The association between liver cancer and diabetes has been a longstanding focus in medical research. Current evidence suggests that diabetes is an independent risk factor for the development of liver cancer. Diabetic retinopathy (DR), a prevalent neurovascular complication of diabetes, has yet to be fully characterised concerning liver cancer. Therefore, this study seeks to identify shared genes and pathways between liver cancer and DR to uncover potential therapeutic targets. Immune infiltration and cell communication in liver cancer were analysed using the GEO single-cell dataset GSM7494113. Single-cell RNA sequencing data from rat retinas were obtained from the GEO datasets GSE209872 and GSE160306. Ferritin phagocytosis-related genes were retrieved from the GeneCards database. The SeuratR package was employed for single-cell clustering analysis, while the CellChat package assessed differences in intercellular communication. Genes shared between DR and liver cancer were identified, and the DGIDB database was consulted to predict potential drug-gene interactions targeting membrane proteins involved in ferritin phagocytosis. Key ferritin phagocytosis (FRHG) genes were further validated using quantitative real-time polymerase chain reaction (qRT-PCR). After annotating the single-cell data through dimensionality reduction and clustering, the expression of genes associated with membrane protein-related ferritinophagy was notably elevated in both HCC and DR samples. Based on the expression of ferritinophagy-related genes, the ferritin deposition score in Müller cells from the DR group was significantly higher than that in the control group. Cell communication analysis revealed that central hub genes associated with ferritinophagy, such as PSAP and MK, along with other signalling pathways, were significantly upregulated in the high Müller group compared to the low Müller group. In contrast, VEGF expression was enhanced in the low Müller group. Importantly, the machine learning model constructed using these key hub genes demonstrated high diagnostic efficacy for both HCC and DR. Finally, by simulating a hyperosmotic diabetic microenvironment, we confirmed in vitro that high glucose conditions significantly stimulate the expression of the shared key hub genes in both HCC and DR. The present study identified the connection between ferritinophagy-related subgroups of cells and key hub genes in both HCC and DR, providing new insights into DR-associated biomarkers and the shared pathological regulatory pathways with HCC. These findings further suggest potential therapeutic targets for both diseases.

Sepsis is defined as a dysregulated host response to infection that results in life-threatening organ dysfunction. The 24-hour urine volume plays a crucial role in assessing the prognosis of septic patients. This study aims to investigate the relationship between 24-hour urine volume and 28-day intensive care unit (ICU) mortality in septic patients and exploring the dose-response relationship between these variables.

This retrospective cohort study analyzed data from 7,218 sepsis patients in the eICU Collaborative Research Database. Logistic regression models and generalized additive models were used to examine the relationship between 24-hour urine volume and 28-day ICU mortality.

A negative correlation was found between 24-hour urine volume and ICU 28-day mortality. In the fully adjusted model, each 50 mL increase in 24-hour urine volume significantly reduced mortality risk by 1% (OR = 0.99, 95% CI = 0.98-0.99, P < 0.001). A nonlinear dose-response relationship was observed, with an inflection point at ~1,663.5 ml. Below this threshold, increased urine volume was significantly associated with reduced mortality risk (OR = 0.97, 95% CI: 0.96-0.98, P < 0.001), while above this point, the relationship was not statistically significant.

This study demonstrates a non-linear negative correlation between 24-hour urine volume and 28-day ICU mortality in sepsis patients.

The retrospective study by Lei et al is an investigation of the relationship between age and subfoveal choroidal thickness (SFCT) in Chinese patients with proliferative diabetic retinopathy. Elements of the study design prevent the generalizability of the study findings, limiting their clinical implications. We recommend consideration of stricter eligibility criteria, other variables like duration of diabetes, interpretation of gender-differences in SFCT, longitudinal follow-up, use of newer choroidal flow indices, comparison of values with normal controls, subgroup analysis to determine the effect of prior treatment, as well as consideration of various real-world scenarios in future studies.