Cardiovascular diseases pose a major threat worldwide. Common cardiovascular diseases include acute myocardial infarction (AMI), heart failure, atrial fibrillation (AF) and atherosclerosis. Glycolysis process often has changed during these cardiovascular diseases. Lactate, the end-product of glycolysis, has been overlooked in the past but has gradually been identified to play major biological functions in recent years. Similarly, the role of lactate in cardiovascular disease is gradually being recognized. Targeting lactate production, regulating lactate transport, and modulating circulating lactate levels may serve as potential strategies for the treatment of cardiovascular diseases in the future. The purpose of this review is to integrate relevant clinical and basic research on the role of lactate in the pathophysiological process of cardiovascular disease in recent years to clarify the important role of lactate in cardiovascular disease and to guide further studies exploring the role of lactate in cardiovascular and other diseases.

Cardiovascular diseases are the leading causes of death worldwide. However, there are still shortcomings in the currently employed treatment methods for these diseases. Therefore, exploring the molecular mechanisms underlying cardiovascular diseases is an important avenue for developing new treatment strategies. Previous studies have confirmed that metabolic and epigenetic alterations are often involved in cardiovascular diseases across patients. Moreover, metabolic and epigenetic factors interact with each other and affect the progression of cardiovascular diseases in a coordinated manner. Lactylation is a novel posttranslational modification (PTM) that links metabolism with epigenetics and affects disease progression. Therefore, analyzing the crosstalk between cellular metabolic and epigenetic factors in cardiovascular diseases is expected to provide insights for the development of new treatment strategies. The purpose of this review is to describe the relationship between metabolic and epigenetic factors in heart development and cardiovascular diseases such as heart failure, myocardial infarction, and atherosclerosis, with a focus on acylation and methylation, and to propose potential therapeutic measures.

• Anti-PD-L1 single-domain antibodies were identified from hPD-L1-immunized camels. • Three novel multifunctional antibodies, anti-PD-L1-CD16a, anti-PD-L1-IL15, and anti-PD-L1-CD16a-IL15, target PD-L1-positive cancer cells. • Anti-PD-L1-IL15 and anti-PD-L1-CD16a-IL15, but not anti-PD-L1-CD16a, stimulate immune cell proliferation in vitro. • The anti-PD-L1 antibodies can bind PD-L1-positive cells. • Anti-PD-L1-CD16a-IL15 has the strongest antitumour activity, both in vitro and in vivo.

Purpose: Our previous data indicated that miR-24-3p is involved in the regulation of vascular endothelial cell (EC) proliferation and migration/invasion. However, whether IL-1β affects hypoxic HUVECs by miR-24-3p is still unclear. Therefore, the present study aimed to investigate the role and underlying mechanism of interleukin 1β (IL-1β) in hypoxic HUVECs. Methods: We assessed the mRNA expression levels of miR-24-3p, hypoxia-inducible factor-1α (HIF1A) and NF-κB-activating protein (NKAP) by quantitative real-time polymerase chain reaction (RT-qPCR). ELISA measured the expression level of IL-1β. Cell counting kit-8 (CCK-8) assays evaluated the effect of miR-24-3p or si-NKAP+miR-24 on cell proliferation (with or without IL-1β). Transwell migration and invasion assays were used to examine the effects of miR-24-3p or si-NKAP+miR-24-3p on cell migration and invasion (with or without IL-1β). Luciferase reporter assays were used to identify the target of miR-24-3p. Results: We demonstrated that in acute myocardial infarction (AMI) patient blood samples, the expression of miR-24-3p is down-regulated, the expression of IL-1β or NKAP is up-regulated, and IL-1β or NKAP is negatively correlated with miR-24-3p. Furthermore, IL-1β promotes hypoxic HUVECs proliferation by down-regulating miR-24-3p. In addition, IL-1β also significantly promotes the migration and invasion of hypoxic HUVECs; overexpression of miR-24-3p can partially rescue hypoxic HUVECs migration and invasion. Furthermore, we discovered that NKAP is a novel target of miR-24-3p in hypoxic HUVECs. Moreover, both the overexpression of miR-24-3p and the suppression of NKAP can inhibit the NF-κB/pro-IL-1β signaling pathway. However, IL-1β mediates suppression of miR-24-3p activity, leading to activation of the NKAP/NF-κB pathway. In conclusion, our results reveal a new function of IL-1β in suppressing miR-24-3p up-regulation of the NKAP/NF-κB pathway.