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Therapeutic Spp1 silencing in TREM2+ cardiac macrophages suppresses atrial fibrillation

Momin, N.; Pabel, S.; Rudra, A.; Kumowski, N.; Lee, I.-H.; Mentkowski, K.; Yamazoe, M.; Stengel, L.; Muse, C. G.; Seung, H.; Paccalet, A.; Gonzalez-Correa, C.; Jacobs, E. B.; Grune, J.; Schloss, M. J.; Sossalla, S.; Wojtkiewicz, G.; Iwamoto, Y.; McMullen, P.; Mitchell, R. N.; Ellinor, P. T.; Anderson, D. G.; Naxerova, K.; Nahrendorf, M.; Hulsmans, M.

2024-08-10 immunology
10.1101/2024.08.10.607461 bioRxiv
Show abstract

Atrial fibrillation (AFib) and the risk of its lethal complications are propelled by fibrosis, which induces electrical heterogeneity and gives rise to reentry circuits. Atrial TREM2+ macrophages secrete osteopontin (encoded by Spp1), a matricellular signaling protein that engenders fibrosis and AFib. Here we show that silencing Spp1 in TREM2+ cardiac macrophages with an antibody-siRNA conjugate reduces atrial fibrosis and suppresses AFib in mice, thus offering a new immunotherapy for the most common arrhythmia.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.