The C1q/TNF superfamily of proteins engages in a pleiotropy of physiological functions associated with various diseases. C1QL proteins demonstrate important protective and regulatory roles in the endocrine, immune, cardiovascular, and nervous systems in both human and rodent studies. Studies in the central nervous system (CNS), adipose, and muscle tissue reveal several C1QL protein and receptor pathways altering multiple cellular responses, including cell fusion, morphology, and adhesion. This review examines C1QL proteins across these systems, summarizing functional and disease associations and highlighting cellular responses based on in vitro and in vivo data, receptor interaction partners, and C1QL-associated protein signaling pathways. We highlight the functions of C1QL proteins in organizing CNS synapses, regulating synapse homeostasis, maintaining excitatory synapses, and mediating signaling and trans-synaptic connections. Yet, while these associations are known, present studies provide insufficient insight into the underlying molecular mechanism of their pleiotropy, including specific protein interactions and functional pathways. Thus, we suggest several areas for more in-depth and interdisciplinary hypothesis testing.
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Phagocytosis involves the engulfment and digestion of detrimental foreign objects (e.g., microbes) by different immune cells of our body, such as macrophages. Lipids play an important role during this immunological process, and hence, microbes have found ways to hijack these lipid pathways during phagocytosis to evade the immune system. For further information, see the review in this issue by Saharan and Kamat, pages 1279–1287. Image provided by Siddhesh Shashikant Kamat.
Pleiotropy of C1QL proteins across physiological systems and their emerging role in synapse homeostasis
Perla A. Peña Palomino, Kylie C. Black, Susanne Ressl; Pleiotropy of C1QL proteins across physiological systems and their emerging role in synapse homeostasis. Biochem Soc Trans 28 June 2023; 51 (3): 937–947. doi: https://doi.org/10.1042/BST20220439
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