Human Anti-Cardiolipin polyclonal antibody

Cardiolipin (CL) was was first identified in bovine heart muscle and was found within the mitochondrial inner membrane, cristae, and inner/outer membrane junctions. It participates in reversing the interior structure of mitochondrial inner membranes, and is vital for cellular energy generation. CL is a significant phospholipid molecule that both forms and maintains the structure and function of mitochondrial and sarcoplasmic reticulum membranes. Normal CL has a symmetrical structure, consisting of a glycerol backbone linked to four acyl groups and carrying two negative charges. This shape maintains the proton gradient across the mitochondrial membrane, affecting enzymes in the oxidative phosphorylation respiratory chain. CL is formed primarily on the membrane of the mitochondria starting from phosphatidic acid.

Figure 1. Major characteristics of cardiolipin (CL)
(Source: Falabella M, et al. 2021)

ACA is the antibody to negative cardiolipins on platelets and endothelial cells. They are antiphospholipid antibodies and one of the signature antibodies of antiphospholipid syndrome. ACA is the immunoglobulin polyclonal which causes disease. It can inhibit thromboxane, promote thrombosis, and affect the functionality of platelets and endothelial cells. Additionally, ACA interferes with the anticoagulant functions of trophoblasts and villous cells, leading to a hypercoagulable state, which can result in recurrent miscarriage and infertility. Research indicates that the simultaneous detection of ACA has clinical significance in predicting cardiac enlargement and heart failure following acute myocardial infarction. In addition, ACA is associated strongly with stroke, autoimmune vasculitis, nephrotic syndrome, connective tissue diseases and infectious diseases.

CL remodeling refers to the loss and disorder of the four fatty acyl chains that make up the cardiolipin molecule. Structural remodeling of CL is commonly observed in chronic diseases. This remodeling is one of the key factors contributing to mitochondrial structural and functional dysfunction associated with chronic non-communicable diseases such as obesity, diabetes, Barth syndrome, and pathological cardiac hypertrophy. The cardiolipin acyltransferase ALCAT1 regulates abnormal CL metabolism by performing remodeling modifications on the branched structure of CL, which accelerates the production of reactive oxygen species, leading to CL remodeling. Therefore, inhibiting CL remodeling is an effective strategy for preventing and treating chronic non-communicable diseases. Different exercise intensities may impact CL metabolism, and exercise could play a role in improving CL remodeling. Research has shown that physical training can increase the expression of CL in both cardiac and skeletal muscles. Additionally, exercise may exert protective effects against ischemic heart disease and diabetes by modulating CL remodeling.

Human Anti-CL polyclonal antibody