Why the study?
S100A8/A9 has emerged as a critical alarmin in nonischaemic cardiomyopathy, prompting an evaluation of its application as a biomarker and therapeutic target for prediction, prevention, and treatment.
S100A8/A9 (Calprotectin) emerges as a promising biomarker and potential therapeutic target in the management of nonischaemic cardiomyopathy.
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May support biomarker exploration in nonischaemic cardiomyopathy; leaves open therapeutic targeting pending prospective trials.
The heterodimeric complex of S100 calcium binding proteins A8 and A9 (S100A8/A9, also known as Calprotectin) is constitutively expressed in myeloid neutrophils and monocytes and plays a role in the modulation of the inflammatory response and cytoskeleton rearrangement. Recently, S100A8/A9 complex has garnered significant attention as a critical alarmin involved in regulating the pathogenesis of various inflammatory cardiovascular diseases, particularly nonischaemic cardiomyopathy (NICM). Furthermore, S100A8/A9 is reportedly associated with the pathophysiological processes of myocardial ischaemia‒reperfusion injury and has also been recognised as a predictor and a potential mediator of heart failure caused by acute myocardial infarction. Recent studies have attempted to provide a comprehensive and detailed overview of the involvement of the S100A8/A9 protein in NICM, covering topics such as hypertrophic myocardial remodelling, septic and dilated cardiomyopathy, myocarditis, chemotherapeutic cardiotoxicity, senescent cardiac dysfunction and cardiac allograft rejection. Ultimately, we aimed to evaluate the application of S100A8/A9 as promising biomarkers and therapeutic strategies for the prediction, prevention and treatment of NICM.
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Lin et al. (2025) studied this question.
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