Cardio-Hematopoietic Axis in Cardiac Injury and Repair: From Adaptation to Maladaptation

The cardiovascular and hematopoietic systems are functionally interconnected through the cardio-hematopoietic axis, a dynamic signaling network that governs hematopoietic responses following cardiac injury. Traditionally viewed primarily as a unidirectional pathway in which cardiac damage mobilizes bone marrow-derived cells to facilitate myocardial repair, emerging evidence now suggests a bidirectional model wherein cardiac-derived cues reciprocally influence hematopoietic stem and progenitor cell fate decisions within the bone marrow niche. This review synthesizes current insights into the mechanistic crosstalk between the injured heart and bone marrow, highlighting the mechanisms by which myocardial injury activates emergency hematopoiesis and immune cell mobilization to support cardiac repair, as well as how cardiac-derived inflammatory and neurohumoral signals remodel the bone marrow niche and reprogram hematopoietic stem cell lineage commitment toward a myeloid-biased, proinflammatory output that amplifies systemic inflammation that contributes to increased cardiovascular risk.

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Publication Details

Journal
Arteriosclerosis Thrombosis and Vascular Biology
Published
2025-11-25
DOI
https://doi.org/10.1161/atvbaha.125.323168
Citations
1
Primary Topic
Cardiac Fibrosis and Remodeling
Type
article
Field-Weighted Citation Impact
1.39
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article

Cardio-Hematopoietic Axis in Cardiac Injury and Repair: From Adaptation to Maladaptation

Douglas L. Mann, Andrew I. Schafer
1 citations
Arteriosclerosis Thrombosis and Vascular Biology
Cardiac Fibrosis and Remodeling
1.39
article

Cardio-Hematopoietic Axis in Cardiac Injury and Repair: From Adaptation to Maladaptation

Douglas L. Mann, Andrew I. Schafer
article en
1 citations

Abstract

The cardiovascular and hematopoietic systems are functionally interconnected through the cardio-hematopoietic axis, a dynamic signaling network that governs hematopoietic responses following cardiac injury. Traditionally viewed primarily as a unidirectional pathway in which cardiac damage mobilizes bone marrow-derived cells to facilitate myocardial repair, emerging evidence now suggests a bidirectional model wherein cardiac-derived cues reciprocally influence hematopoietic stem and progenitor cell fate decisions within the bone marrow niche. This review synthesizes current insights into the mechanistic crosstalk between the injured heart and bone marrow, highlighting the mechanisms by which myocardial injury activates emergency hematopoiesis and immune cell mobilization to support cardiac repair, as well as how cardiac-derived inflammatory and neurohumoral signals remodel the bone marrow niche and reprogram hematopoietic stem cell lineage commitment toward a myeloid-biased, proinflammatory output that amplifies systemic inflammation that contributes to increased cardiovascular risk.

Arteriosclerosis Thrombosis and Vascular BiologyVol. 46(1)
Washington University in St. Louis (US), Cornell University (US), Presbyterian Hospital (US), Cardiovascular Research Center (BR)
Openalex Percentile: Top 13%
Cardiac Fibrosis and Remodeling
1.39
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