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Cardiac fibroblasts play a pivotal role in maintaining heart homeostasis by depositing extracellular matrix (ECM) to provide structural support for the myocardium, vasculature, and neuronal network and by contributing to essential physiological processes. In response to injury such as myocardial infarction or pressure overload, fibroblasts become activated, leading to increased ECM production that can ultimately drive left ventricular remodeling and progress to heart failure. Recently, the American Journal of Physiology-Heart and Circulatory Physiology issued a call for papers on cardiac fibroblasts that yielded articles with topics spanning fibroblast physiology, technical considerations, signaling pathways, and interactions with other cell types. This mini-review summarizes those articles and places the new findings in the context of what is currently known for cardiac fibroblasts and what future directions remain. [ABSTRACT FROM AUTHOR]

Gallium-68 fibroblast activation protein inhibitor [(68Ga)Ga-FAPI] is a new radiopharmaceutical positioning itself as the preferred agent in patients with malignant tumours, competing with 2-Deoxy-2-[18F]fluoro-d-glucose [2-(18F) FDG] using positron emission tomography (PET). While imaging oncology patients with [68Ga]Ga-FAPI PET, incidental uptake of [68Ga]Ga-FAPI has been detected in the myocardium. This review summarises original research studies associating the visualisation of FAPI-based tracers in the myocardium with underlying active cardiovascular disease. [ABSTRACT FROM AUTHOR]