Cassandra P Awgulewitsch1,2, Linh T Trinh1,2, Antonis K Hatzopoulos3,4. 1. Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2213 Garland Avenue, Nashville, TN, 37232-6300, USA. 2. Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA. 3. Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2213 Garland Avenue, Nashville, TN, 37232-6300, USA. antonis.hatzopoulos@vanderbilt.edu. 4. Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA. antonis.hatzopoulos@vanderbilt.edu.
Abstract
PURPOSE OF REVIEW: This review aims to summarize recent findings regarding the plasticity and fate switching among somatic and progenitor cells residing in the vascular wall of blood vessels in health and disease. RECENT FINDINGS: Cell lineage tracing methods have identified multiple origins of stem cells, macrophages, and matrix-producing cells that become mobilized after acute or chronic injury of cardiovascular tissues. These studies also revealed that in the disease environment, resident somatic cells become plastic, thereby changing their stereotypical identities to adopt proinflammatory and profibrotic phenotypes. Currently, the functional significance of this heterogeneity among reparative cells is unknown. Furthermore, mechanisms that control cellular plasticity and fate decisions in the disease environment are poorly understood. Cardiovascular diseases are responsible for the majority of deaths worldwide. From a therapeutic perspective, these novel discoveries may identify new targets to improve the repair and regeneration of the cardiovascular system.
PURPOSE OF REVIEW: This review aims to summarize recent findings regarding the plasticity and fate switching among somatic and progenitor cells residing in the vascular wall of blood vessels in health and disease. RECENT FINDINGS: Cell lineage tracing methods have identified multiple origins of stem cells, macrophages, and matrix-producing cells that become mobilized after acute or chronic injury of cardiovascular tissues. These studies also revealed that in the disease environment, resident somatic cells become plastic, thereby changing their stereotypical identities to adopt proinflammatory and profibrotic phenotypes. Currently, the functional significance of this heterogeneity among reparative cells is unknown. Furthermore, mechanisms that control cellular plasticity and fate decisions in the disease environment are poorly understood. Cardiovascular diseases are responsible for the majority of deaths worldwide. From a therapeutic perspective, these novel discoveries may identify new targets to improve the repair and regeneration of the cardiovascular system.
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