Patients recovered from COVID-19 present loss of the ΔΨ_m in HPBMC, leading to mitochondrial dysfunction, which is associated with the onset and progression of several chronic diseases such as pulmonary fibrosis, Alzheimer's, Parkinson's, and multiple sclerosis. Therefore, determining the ΔΨ_m in patients recovered from SARS-CoV-2 could be an early sign of several diseases caused by post-COVID-19 sequelae.

This work describes a novel mechanism of acute leukemia regulation mediated by tumor miRNAs driving a pro-inflammatory microenvironment and hematopoietic cell activation by TLR signals

Review of how flavonoids control microglial activation states through regulation of microRNAs and the implications in Alzheimer's disease appearance and progression.

Clinical and molecular evidence of putative interactions between β- and γ-herpesviruses that cause or worsen pathological disorders

Neuroimmunoendocrinology is has established its place as a biomedical discipline worldwide in the past 70 years.

Sophoridine may inhibit endotoxin-induced ALI by enhancing the autophagy of macrophages and reducing inflammation. The mechanism may be related to sophoridine downregulated the expression of TLR4/MyD88/NF and mTOR.

A high-calorie diet can potentially reset the gut microbiome and metabolites, disrupt Th17/Treg cell balance and aggravate LPS-induced lung inflammatory damage.

Kakonein reduced the release of lysosomal cathepsin B and consequently inhibited NLRP3 inflammasome activation to prevent hyperglycaemia-associated dysfunction of macrophage digestion.

K48 and K27 ubiquitination contribute to regulating immune function of bone marrow precursor cells by affecting cross-presentation and thereby might be therapeutic target