Microglia are unique brain-resident, myeloid cells. They have received growing interest for their implication in an increasing number of neurodevelopmental, acute injury, and neurodegenerative disorders of the central nervous system (CNS). Fate-mapping studies establish microglial ontogeny from the periphery during development, while recent transcriptomic studies highlight microglial identity as distinct from other CNS cells and peripheral myeloid cells. This evidence for a unique microglial ontogeny and identity raises questions regarding their identity and functions across species. This review will examine the available evidence for microglia in invertebrate and vertebrate species to clarify similarities and differences in microglial identity, ontogeny, and physiology across species. This discussion highlights conserved and divergent microglial properties through evolution. Finally, we suggest several interesting research directions from an evolutionary perspective to adequately understand the significance of microglia emergence. A proper appreciation of microglia from this perspective could inform the development of specific therapies geared at targeting microglia in various pathologies.
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http://dx.doi.org/10.3389/fcell.2021.652748 | DOI Listing |
J Transl Med
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Background: Dilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Infiltration and alterations in non-cardiomyocytes of the human heart involve crucially in the occurrence of DCM and associated immunotherapeutic approaches.
Methods: We constructed a single-cell transcriptional atlas of DCM and normal patients.
Mol Cancer
January 2025
Department of Hematology, Qilu Hospital of Shandong University, No.117, West of Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.
Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.
Sci Rep
January 2025
Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Acute rejection (AR) is a significant complication in liver transplantation, impacting graft function and patient survival. Kupffer cells (KCs), liver-specific macrophages, can polarize into pro-inflammatory M1 or anti-inflammatory M2 phenotypes, both of which critically influence AR outcomes. Angiopoietin-like 4 (ANGPTL4), a secretory protein, is recognized for its function in regulating inflammation and macrophage polarization.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Göttingen, Germany.
Pancreatic ductal adenocarcinoma (PDAC) displays a high degree of spatial subtype heterogeneity and co-existence, linked to a diverse microenvironment and worse clinical outcome. However, the underlying mechanisms remain unclear. Here, by combining preclinical models, multi-center clinical, transcriptomic, proteomic, and patient bioimaging data, we identify an interplay between neoplastic intrinsic AP1 transcription factor dichotomy and extrinsic macrophages driving subtype co-existence and an immunosuppressive microenvironment.
View Article and Find Full Text PDFPhysiol Rep
January 2025
Department of Medicine, John A. Burns School of Medicine, University of Hawaii Mānoa, Honolulu, Hawaii, USA.
Inflammation and a metabolic shift from oxidative metabolism to glycolysis are common in the ischemic heart, the latter partly controlled by pyruvate kinase (muscle, PKM). We previously identified alternative splicing promoting the PKM2 isoform after myocardial infarction (MI). We examined the role of PKM2 physiological upregulation after MI, modeled by ligation of the left anterior descending coronary artery, using global PKM2 knockout (PKM2) mice.
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