We are analyzing https://link.springer.com/article/10.1007/s00395-021-00897-1.

Title:
Resolving the intertwining of inflammation and fibrosis in human heart failure at single-cell level | Basic Research in Cardiology
Description:
Inflammation and fibrosis are intertwined mechanisms fundamentally involved in heart failure. Detailed deciphering gene expression perturbations and cell–cell interactions of leukocytes and non-myocytes is required to understand cell-type-specific pathology in the failing human myocardium. To this end, we performed single-cell RNA sequencing and single T cell receptor sequencing of 200,615 cells in both human dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) hearts. We sampled both lesion and mild-lesion tissues from each heart to sequentially capture cellular and molecular alterations to different extents of cardiac fibrosis. By which, left (lesion) and right ventricle (mild-lesion) for DCM hearts were harvest while infarcted (lesion) and non-infarcted area (mild-lesion) were dissected from ICM hearts. A novel transcription factor AEBP1 was identified as a crucial cardiac fibrosis regulator in ACTA2+ myofibroblasts. Within fibrotic myocardium, an infiltration of a considerable number of leukocytes was witnessed, especially cytotoxic and exhausted CD8+ T cells and pro-inflammatory CD4+ T cells. Furthermore, a subset of tissue-resident macrophage, CXCL8hiCCR2+HLA-DRhi macrophage was particularly identified in severely fibrotic area, which interacted with activated endothelial cell via DARC, that potentially facilitate leukocyte recruitment and infiltration in human heart failure.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, heart, wang, failure, singlecell, human, cells, chen, zhang, cell, cardiac, nat, httpsdoiorgs, fibrosis, nature, beijing, supplementary, guo, med, china, inflammation, endothelial, myocardial, transcriptional, file, data, research, cellular, factor, macrophage, res, macrophages, circulation, immunol, reveals, university, xlsx, privacy, cookies, content, information, basic, rao, sequencing, inflammatory,

Topics {✒️}

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      description:Inflammation and fibrosis are intertwined mechanisms fundamentally involved in heart failure. Detailed deciphering gene expression perturbations and cell–cell interactions of leukocytes and non-myocytes is required to understand cell-type-specific pathology in the failing human myocardium. To this end, we performed single-cell RNA sequencing and single T cell receptor sequencing of 200,615 cells in both human dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) hearts. We sampled both lesion and mild-lesion tissues from each heart to sequentially capture cellular and molecular alterations to different extents of cardiac fibrosis. By which, left (lesion) and right ventricle (mild-lesion) for DCM hearts were harvest while infarcted (lesion) and non-infarcted area (mild-lesion) were dissected from ICM hearts. A novel transcription factor AEBP1 was identified as a crucial cardiac fibrosis regulator in ACTA2+ myofibroblasts. Within fibrotic myocardium, an infiltration of a considerable number of leukocytes was witnessed, especially cytotoxic and exhausted CD8+ T cells and pro-inflammatory CD4+ T cells. Furthermore, a subset of tissue-resident macrophage, CXCL8hiCCR2+HLA-DRhi macrophage was particularly identified in severely fibrotic area, which interacted with activated endothelial cell via DARC, that potentially facilitate leukocyte recruitment and infiltration in human heart failure.
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      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:Department of Thoracic Surgery, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:BIOPIC and School of Life Sciences, Peking University, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:National Clinical Research Center for Orthopedics, Sports Medicine and Rehabilitation, General Hospital of Chinese PLA, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:BIOPIC and School of Life Sciences, Peking University, Beijing, China
      name:Beijing Advanced Innovation Center for Genomics, Peking University, Beijing, China
      name:Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:BIOPIC and School of Life Sciences, Peking University, Beijing, China
      name:Analytical Biosciences Limited, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
      name:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science, PUMC, Beijing, China
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