Pulmonary fibrosis, a critical outcome of chronic inflammatory diseases, has gained prominence in the context of post-coronavirus (post-COVID-19) complications. This review delves into the multifaceted landscape of post-COVID-19 pulmonary fibrosis, elucidating the intricate molecular mechanisms underlying its pathogenesis and highlighting promising therapeutic avenues. Examining the aftermath of severe acute respiratory syndrome-2 (SARS-CoV-2) infection, the review reveals key signaling pathways implicated in the fibrotic cascade. Drawing parallels with previous coronavirus outbreaks enhances our understanding of the distinctive features of post-COVID-19 fibrosis. Antifibrotic drugs, like pirfenidone and nintedanib, take center stage; their mechanisms of action and potential applications in post-COVID-19 cases are thoroughly explored. Beyond the established treatments, this review investigates emerging therapeutic modalities, including anti-interleukin agents, immunosuppressants, and experimental compounds, like buloxybutide, saracatinib, sirolimus, and resveratrol. Emphasizing the critical importance of early intervention, this review highlights the dynamic nature of post-COVID-19 pulmonary fibrosis research. In conclusion, the synthesis of current knowledge offers a foundation for advancing our approaches to the prevention and treatment of these consequential sequelae of COVID-19.

Obesity is a major public health problem that puts pressure on healthcare systems globally. The purpose of this narrative review is to summarize and analyse recent research on the bidirectional link between obesity and mental health, focusing on the biological, behavioural, dietary, emotional, and metabolic mechanisms arising from gut microbiota interactions. Epidemiological association between obesity and mental health disorders, especially depression and anxiety, often occurs bidirectionally, reinforcing each other. Low-grade systemic inflammation is a condition typically found in obesity, being a fundamental element of neuropsychiatric disorders. Considered the main energy substrate for colon cells, SCFAs are synthesized in the intestine and exert important local effects by reducing both local and systemic inflammation. The intestinal microbiota maintains this homeostasis through the SCFAs it produces. The combined impact of the increased intestinal permeability, immune activation, and disrupted metabolism of SCFAs and tryptophan contributes to the onset and progression of depression and anxiety, as well as to significant cognitive dysfunction, especially in obese individuals. Understanding the mechanisms by which microbiota metabolites influence brain development, neuroplasticity, and behaviour could pave the way for new and innovative therapeutic strategies for the treatment of obesity and depression. Conclusions: The association of these pathologies is not coincidental, as they coexist through overlapping biological pathways that they partially or completely share. The main pathway involved is formed by the brain–gut axis and its mediators (SCFAs).

Objectives: Post-acute venous thromboembolism (VTE) is a well-recognized complication of COVID-19, driven by persistent endothelial dysfunction and thromboinflammation. Identifying simple clinical predictors of VTE may optimize therapy and limit adverse outcomes. We propose a pragmatic risk-stratification approach, based on clinical and echocardiographic parameters. Methods: We conducted a retrospective cohort study in a Romanian tertiary hospital (March 2020–April 2022) in 54 adults with laboratory-confirmed COVID-19 and imaging-confirmed VTE. Demographics, comorbidities, laboratory markers, and echocardiographic variables—particularly tricuspid annular plane systolic excursion (TAPSE), peripheral oxygen saturation (SpO₂), and left-ventricular end-diastolic diameter (LVEDD)—were collected. The primary outcome was the percentage of patients receiving systemic thrombolysis. Statistical analyses included Mann–Whitney U tests, chi-square, Spearman correlations, and multivariable logistic regression. Results: The mean age was 61.2 ± 14.7 years, and 63% were men. Eleven patients (20.4%) underwent thrombolysis. Compared with conservatively managed patients, those receiving thrombolysis had lower TAPSE (13.0 vs. 20.8 mm), lower SpO₂ (90.1 vs. 97.0%), and smaller LVEDD (24.4 vs. 46.1 mm); all differences were statistically significant. Each 1 mm decrease in TAPSE and 1% decrease in SpO₂ increased the likelihood of thrombolysis (adjusted odds ratios 1.58 and 1.34, respectively). Inflammatory markers and right-ventricular diameter were not associated with treatment. Conclusions: Reduced TAPSE, lower SpO₂, and decreased LVEDD identify post-COVID VTE patients at elevated risk of hemodynamic compromise requiring thrombolysis. A point-of-care assessment incorporating these variables may improve early risk stratification and guide therapeutic decisions.