Cellular cross-talks in the diseased and aging heart
Key result
Cellular cross-talks between immune cells, endothelial cells, fibroblasts, and cardiomyocytes mediate cardiac dysfunction, aging, and repair mechanisms in the heart.
Why the study?
Altered cellular cross-talk during disease and aging drives cardiac remodeling, but adaptive cellular changes can also mediate repair and regeneration.
Design
Review
Authors
Discussion
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Implication
Informs preclinical models of cardiac aging and repair; leaves open translation to clinical interventions.
Key Points
- To review the signaling networks and cellular interactions among cardiomyocytes, fibroblasts, endothelial cells, and immune cells that govern cardiac aging, dysfunction, and post-injury repair.
- Synthesized molecular and cellular evidence detailing cell-to-cell communication in physiological and pathological cardiac states.
- Examined phenotypic shifts across specialized cardiac cell subpopulations during tissue remodeling, heart failure progression, and endogenous regeneration.
- Cellular heterogeneity coordinates essential baseline cardiac functions through synchronized cross-talk between structural, vascular, and immune cells.
- Aging and chronic cardiovascular disease disrupt normal intercellular communication, accelerating maladaptive tissue remodeling and heart failure.
- Phenotypic activation of reparative cell subsets, specifically reparative macrophages and fibroblasts, promotes endogenous wound healing and cardiac tissue regeneration.
PICO
P
Population
Heart failure and cardiac aging
E
Exposure / Comparator
Cellular cross-talks
This review summarizes the complex intercellular communication networks in the heart that drive both pathological remodeling and regenerative repair during aging and disease.
Cite This Study
Wagner et al. (2019) conducted a review in Heart failure and cardiac aging. Cellular cross-talks was evaluated. Cellular cross-talks between immune cells, endothelial cells, fibroblasts, and cardiomyocytes mediate cardiac dysfunction, aging, and repair mechanisms in the heart.