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Copper (Cuprum) is an essential trace metal indispensable for the function of numerous enzymatic molecules implicated in cellular metabolism. Emerging evidence has demonstrated the role of copper in angiogenesis and cellular signaling. Moreover, raised copper levels have been detected in hepatocellular carcinoma and other cancers. An inherited or acquired copper imbalance, including inadequately low or excessively high copper levels, as well as inappropriate copper distribution in the body, is implicated in a number of diseases. In addition, a recent groundbreaking study identified a copper-induced type of programmed cell death named cuprotosis, the mechanism of which greatly deferred from that of other known cell death modes. The first part provides an overview of the regulation of copper homeostasis and discusses the underlying mechanisms of cuprotosis. In the second part, the authors focus on the functions of copper in liver diseases and other metabolic disorders, before discussing how this knowledge could contribute to the development of effective targets to treat such diseases.

Low-density lipoprotein cholesterol (LDL-C) is the most important risk factor for atherosclerotic cardiovascular disease (ASCVD), but some individuals who meet the LDL-C treatment goal still have a residual risk of ASCVD [1]. Numerous clinical studies and meta-analyses have shown that high lipoprotein (a) (Lp(a)) concentration is a continuous, independent, and moderately significant risk factor for ASCVD, and that this association is not dependent on LDL-C or non-HDL-C levels or other risk factors [2].

Lp(a) was first introduced to the scientific world by the Norwegian physician and geneticist Kare Berg in 1963 [3]. Lp(a) closely resembles LDL in terms of its protein and lipid composition, containing one molecule of apolipoprotein B (apoB) wrapped around a core of cholesterol esters and triglycerides with a surface of phospholipids and unesterified cholesterol particles. Lp(a) also contains a highly glycosylated protein called apo(a). This protein forms a covalent bond with apoB-100 via a single disulfide bond, which distinguishes Lp(a) from LDL.

Despite the fact that the structure of Lp(a) is similar to that of LDL, Lp(a) with a unique apo(a) is more atherogenic than LDL, and it is an attractive target for blood lipid intervention. The expert panel of the Beijing Heart Society has extended the systematic knowledge regarding Lp(a) beyond integrating the current global knowledge of Lp(a) and summarizing the evidence from Chinese populations. The scientific statement from Beijing Heart Society suggests key points for managing Lp(a) in Chinese populations for reference in clinical practice [4].

Lp(a) concentrations vary greatly among different races and geographic regions. In the Chinese population, Lp(a) concentrations have a skewed distribution with a median concentration of 5.6–8.0 mg/dL, which is slightly lower than that in Caucasians (9.0–17.0 mg/dL) but much lower than that in African Americans (33 mg/dL). Lp(a) concentrations are heritable, with total heritability of 68%–98%. The LPA gene (MIM 152200; ENSG00000198670) located on chromosome 6q27 encodes apo(a), and copy number variations in KIV-2 within the gene can range from 2 to 40 copies, which can explain 70%–90% of plasma Lp(a) concentrations [5].

In addition, single-nucleotide polymorphisms on the LPA gene are also associated with Lp(a) concentrations. The variant rs10455872 located in intron 25 and rs3798220 in the protease-like domain show the strongest correlation with Lp(a) concentrations, accounting for 22% of the variation in Lp(a) concentrations. However, these two single-nucleotide polymorphisms have not been found to be associated with Lp(a) concentrations in South Asian and Chinese populations [6]. In Chinese populations, rs7770628 and rs73596816 are the single-nucleotide polymorphisms most significantly associated with the severity of coronary heart disease in Chinese pati

Influenza A infection leads to a higher incidence of liver injury in HBV carriers than in patients infected with influenza A alone. Moreover, HBV carriers experience earlier onset and greater severity of liver injury than individuals with only influenza A.

Autoantibody (AAb) detection has become one of the standards of diagnosis for autoimmune liver disease (AILD), and some AAbs have become specific biomarkers of AILD. In addition, AAbs can be detected in patients with non-AILDs, such as viral hepatitis and alcoholic liver disease. However, the distribution characteristics and pathogenic mechanisms of AAbs in patients with non-AILD are unclear. This article summarizes the characteristics of AAbs in several common clinical chronic liver diseases (CLDs) and discusses the value of AAb analysis in CLD.

SARS-CoV-2 infections have an increased risk of developing severe disease and a variety of secondary bacterial or fungal infections, and the types of microbiology testing of specimens vary accordingly. A standardized process of specimen collection and handling contributes to the correct diagnosis and treatment of patients with COVID-19.

Chimeric antigen receptor (CAR) T cell therapy is a relatively new form of targeted therapy that has demonstrated impressive success in treating hematological malignancies. It has been challenging to translate this success to solid tumors. Reasons for this include barriers to delivery, tumor heterogeneity, cancer cells' ability to evade the immune system as well as identifying the optimal target. Most CAR T clinical trials have targeted well-characterized cancer targets with significant preclinical and in some cases clinical validation. Published results from some of these trials show signs of anti-cancer activity that warrant encouragement, but also caution, given instances of unacceptable toxicity. The narrow therapeutic window is complicated by the ability of CAR T cells to expand in patients regardless of dose. Here, we review those trials showing encouraging results in the context of target selection. It is clear that more specific tumor targeting is required, either by affinity tuning to avoid low-level target expression in healthy cells, logic gating, or the identification of new targets that are more cancer specific.