Key result
Recombinant RELMα delays heart failure onset, while loss of Retnla accelerates progression.
Why the study?
Does administration of RELMα or modulation of TIMD4hiMHCⅡhi macrophages affect heart failure progression in preclinical models?
Does administration of RELMα or modulation of TIMD4hiMHCⅡhi macrophages affect heart failure progression in preclinical models?
Answers are grounded in this paper and cite their sources.
TIMD4hiMHCⅡhi macrophages and their signature gene Retnla (RELMα) play a protective role in delaying heart failure progression.
Genetic fate mapping confirmed the existence of the TIMD4hiMHCⅡhi macrophage subset and showed that they were resident macrophages with minimal input from peripheral monocytes. Further, single-cell RNA sequencing revealed that Retnla could serve as the signature gene for TIMD4hiMHCⅡhi macrophages. Administration of recombinant protein of the Retnla gene, RELMα, delayed the onset of heart failure, whereas either deletion of TIMD4hiMHCⅡhi macrophages or macrophage-specific loss of Retnla facilitated heart failure progression.
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Zhang et al. (2024) studied Heart failure. Recombinant protein RELMα (Retnla) was evaluated on Onset and progression of heart failure. Administration of recombinant RELMα delayed the onset of heart failure, whereas deletion of TIMD4hiMHCⅡhi macrophages or loss of Retnla facilitated heart failure progression.
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