Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secretory serine protease synthesized primarily by the liver. It mainly promotes the degradation of low-density lipoprotein receptor (LDL-R) by binding LDL-R, reducing low-density lipoprotein cholesterol (LDL-C) clearance. In addition to regulating LDL-R, PCSK9 inhibitors can also bind Toll-like receptors (TLRs), scavenger receptor B (SR-B/CD36), low-density lipoprotein receptor-related protein 1 (LRP1), apolipoprotein E receptor-2 (ApoER2) and very-low-density lipoprotein receptor (VLDL-R) reducing the lipoprotein concentration and slowing thrombosis. In addition to cardiovascular diseases, PCSK9 is also used in pancreatic cancer, sepsis, and Parkinson’s disease. Currently marketed PCSK9 inhibitors include alirocumab, evolocumab, and inclisiran, as well as small molecules, nucleic acid drugs, and vaccines under development. This review systematically summarized the application, preclinical studies, safety, mechanism of action, and latest research progress of PCSK9 inhibitors, aiming to provide ideas for the drug research and development and the clinical application of PCSK9 in cardiovascular diseases and expand its application in other diseases.

Psoriasis (PSO) is a common skin disease affecting approximately 1%–3% of the population, and the incidence rate is increasing yearly. PSO is associated with a dramatically increased risk of cardiovascular disease, the most common of which is atherosclerosis (AS). In the past, inflammation was considered to be the triggering factor of the two comorbidities, but in recent years, studies have found that lipid metabolism disorders increase the probability of atherosclerosis in patients with psoriasis. In this review, we discuss epidemiological studies, clinical treatment methods, risk factors, and lipid metabolism of psoriasis and atherosclerosis comorbidities.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic, symmetric polyarticular synovitis, with a global prevalence of approximately 0.5%-1%. Its pathogenesis involves a complex interplay of genetic and environmental factors, as well as abnormal immune activation. RA patients face a significantly increased risk of cardiovascular disease, with atherosclerosis (AS) and its complications being the leading cause of mortality. Chronic systemic inflammation has long been considered the core pathological bridge linking RA and AS, whereby inflammatory cytokines drive cardiovascular events by impairing endothelial function and promoting arterial plaque formation and destabilization. However, recent research has yielded critical breakthroughs, revealing that dyslipidemia plays a vital role in RA pathogenesis and its comorbidity with AS. It goes beyond a traditional secondary effect, serving as an active participant intertwined with the immune-inflammatory network. This review specifically focuses on lipid-immune crosstalk in RA-AS comorbidity. To this end, we aim to systematically outline the epidemiological evidence for this association, summarize current clinical management strategies and their impact on cardiovascular risk, analyze shared risk factors, and explore in depth the central role of lipid metabolism in their shared pathophysiological mechanisms. We focus on cutting-edge topics such as the “lipid paradox” phenomenon, lipoprotein dysfunction, lipid metabolic dysregulation in macrophages and the imbalance of bioactive lipid mediators to provide a comprehensive perspective and theoretical basis for understanding their common pathophysiological pathways and developing novel therapeutic strategies targeting the metabolism-immune axis.

Lung ischemia-reperfusion injury is a major complication after lung transplantation and is closely associated with oxidative stress, inflammatory amplifica