{"doi":"10.3389/fimmu.2023.1215855","title":"Inhibition of NK1.1 signaling attenuates pressure overload-induced heart failure, and consequent pulmonary inflammation and remodeling","abstract":"Background: Inflammation contributes to heart failure (HF) development, the progression from left ventricular failure to pulmonary remodeling, and the consequent right ventricular hypertrophy and failure. NK1.1 plays a critical role in Natural killer (NK) and NK T (NKT) cells, but the role of NK1.1 in HF development and progression is unknown. Methods: We studied the effects of NK1.1 inhibition on transverse aortic constriction (TAC)-induced cardiopulmonary inflammation, HF development, and HF progression in immunocompetent male mice of C57BL/6J background. Results: NKT cells in peripheral blood, spleen, and lung tissues, but had no effect on cardiopulmonary structure and function under control conditions. However, systemic inhibition of NK1.1 signaling by anti-NK1.1 antibodies significantly rescued mice from TAC-induced left ventricular inflammation, fibrosis, and failure. Inhibition of NK1.1 signaling also significantly attenuated TAC-induced pulmonary leukocyte infiltration, fibrosis, vessel remodeling, and consequent right ventricular hypertrophy. Moreover, inhibition of NK1.1 signaling significantly reduced TAC-induced pulmonary macrophage and dendritic cell infiltration and activation. Conclusions: Our data suggest that inhibition of NK1.1 signaling is effective in attenuating systolic overload-induced cardiac fibrosis, dysfunction, and consequent pulmonary remodeling in immunocompetent mice through modulating the cardiopulmonary inflammatory response.","journal":"Frontiers in Immunology","year":2023,"id":349843,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":10,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.962,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1093367,"name":"Rui Xu","orcid":"0000-0001-6236-4529","position":1,"is_corresponding":false},{"id":1093368,"name":"Lihong Pan","orcid":"0000-0002-1995-2373","position":2,"is_corresponding":false},{"id":425922,"name":"Umesh Bhattarai","orcid":"0009-0003-4042-836X","position":3,"is_corresponding":false},{"id":456837,"name":"Xiaoguang Liu","orcid":"0000-0003-0183-2100","position":4,"is_corresponding":false},{"id":374442,"name":"Heng Zeng","orcid":"0000-0001-8559-2807","position":5,"is_corresponding":false},{"id":374444,"name":"Jian‐Xiong Chen","orcid":"0000-0001-9203-4336","position":6,"is_corresponding":false},{"id":24967,"name":"Michael E. Hall","orcid":"0000-0002-5733-1025","position":7,"is_corresponding":false},{"id":784544,"name":"Yingjie Chen","orcid":"0000-0002-4059-7847","position":8,"is_corresponding":false},{"id":374443,"name":"Xiaochen He","orcid":"0000-0002-8266-5895","position":0,"is_corresponding":true}],"reference_count":48,"raw_metadata":null,"created_at":"2026-07-19T01:12:19.059218Z","pmid":"37554327","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}