{"doi":"10.3389/fcvm.2023.1195863","title":"Editorial: The role of inflammation, stem cells and progenitor cells in cardiovascular repair","abstract":"inflammation turns into a damaging phenomenon for the host organism. These aspects are objects of the articles contributing to this collection that are briefly summarized in this editorial. Li et al. reviewed and discussed the two-sided roles of the cells involved in inflammation. Kumar et al. demonstrate biphasic kinetics of CD4 + T-lymphocytes after MI using animal models. Yang et al. identified PFKFB2 as a key gene for the transition from acute to old MI in humans. The interaction between diabetes and MI is studied by Baumbach et al. who investigated CD34 + /CXCR4 + cells in diabetic MI.Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated by Li et al. Cardiac inflammation and the timely resolution of inflammatory processes are critical to prevent adverse cardiac remodeling and heart failure. After myocardial infarction, neutrophils first arrive at the damage site within 6-24 hours followed by monocytes and macrophages, which contribute to myocardial cell death and injury. Then, monocyte, macrophages, and regulatory T cells are recruited and produce anti-inflammatory mediators and resolvins to promote cardiac repair. In this process, other cells such as fibroblasts can influence the immune cells bya paracrine effect of TGF-β. Neutrophils and macrophages have two-sided roles (pro-inflammatory and anti-inflammatory) depending on the cellular subtypes (N1 and N2 for neutrophils, M1 and M2 for macrophages). Interestingly, non-coding RNAs and epigenetic modifications regulate the fate of immune cells either pro-inflammatory or anti-inflammatory in the cardiac environment. They concluded that these anti-inflammatory drugs, non-coding RNAs, and epigenetic modulatorscould be the target for MI therapy. CD4 + T-lymphocytes exhibit biphasic kinetics post-myocardial infarction.In this manuscript, Kumar et al. report preclinical data collected in mice that shed new light on the ongoing debate on the acute versus chronic effects of CD4 + T cells in post-MI physiopathological events. It is known that mice lacking CD4 + (global CD4 -/animals) are defective in myocardial healing after acute myocardial infarction (MI) and show increased mortality (1). On the other hand, CD4 + T cells are important in cardiac remodeling during heart failure (HF) (2). Therefore, it is of high relevance to dissect the T-cell responses to wound healing (in MI) vs. tissue remodeling (in HF). The study presented in this article reveals that T-cell phenotype and activation state is different in MI vs HF. In the HF model, the transmigration of all T-cell subsets (Th1, Th2, Th17, and Tregs) is bi-phasic during HF. Furthermore, authors introduced Rosa26-iDTR (inducible Diohteria Toxin Receptor) to CD4-cre mice and demonstrated that the depletion of CD4 + T cells at the second phase of transmigration significantly inhibited the LV remodeling and increase of end-systolic and end-diastolic volumes (EDV and ESV) during MI.Thus new studies dedicated to the associated molecular mechanisms are warranted.Identification of PFKFB2 as a key gene for the transition from acute to old myocardial infarction in peripheral blood, Post-MI inflammatory and metabolic pathways play a significant role in deciding the fate of structural and functional properties of the injured heart to HF. However, it is unclear how the initial immuno-metabolic response during acute MI (AMI) evolves over a period of time (old MI; OMI) during the progression of HF. In this manuscript, Yang et al. provide valuable insights into the signaling pathways impacted by circulating immune cells during the transition from acute AMI to a more advanced OMI. Using Cibersoft, WGCNA, and Random Forest Model, they identified a key glyclosis gene, PFKFB2 that seemed to associate with the differential distribution of immune cells. They found low expression levels of PFKFB2 in peripheral blood cells from OMI samples compared to AMI samples. The authors suggest that PFKFB2 can help predict the di","journal":"Frontiers in Cardiovascular Medicine","year":2023,"id":399076,"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":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9515,"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":1175183,"name":"Antonino Bruno","orcid":"0000-0002-4790-0861","position":1,"is_corresponding":false},{"id":254368,"name":"Prabhakara R. Nagareddy","orcid":"0000-0002-0294-641X","position":2,"is_corresponding":false},{"id":399555,"name":"Toshio Nakanishi","orcid":"0000-0002-7374-9317","position":3,"is_corresponding":false},{"id":230183,"name":"Murugesan V. S. Rajaram","orcid":"0000-0002-1515-1122","position":4,"is_corresponding":false},{"id":1175184,"name":"Gaia Spinetti","orcid":"0000-0001-7996-6809","position":5,"is_corresponding":false},{"id":1175182,"name":"Nanako Kawaguchi","orcid":"0000-0002-6518-3181","position":0,"is_corresponding":true}],"reference_count":4,"raw_metadata":null,"created_at":"2026-07-19T01:19:51.724387Z","pmid":"37144059","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":[]}