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Beyond Unidirectional Injury: Bidirectional Interactions Between Arteriosclerosis and the Heart-Brain-Kidney Axis
1Department of Anesthesiology, Perioperative and Pain Medicine, Nanjing First Hospital, Nanjing Medical University, Jiangsu, China.
Insights
Arteriosclerosis, a vascular disorder linked to aging and hypertension, damages organs like the heart, brain, and kidneys. Organ damage then worsens arteriosclerosis, creating a harmful cycle.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Gerontology
Background:
- Arteriosclerosis is a systemic degenerative vascular disorder.
- Characterized by arterial wall thickening, reduced elasticity (arterial stiffness), and luminal narrowing.
- Closely associated with aging and hypertension.
Purpose of the Study:
- To summarize mechanisms by which arteriosclerosis drives multi-organ damage.
- To highlight clinical manifestations and outcomes of arteriosclerosis-related organ damage.
- To discuss the feedback loop between target organ dysfunction and worsening vascular disease.
Main Methods:
- Literature review of arteriosclerosis mechanisms.
- Analysis of pathological processes: lipid deposition, inflammation, calcification, hemodynamic disturbances.
- Examination of vascular-organ interactions and feedback pathways.
Main Results:
- Arteriosclerosis progressively injures high metabolic demand organs (heart, brain, kidneys).
- Organ injury activates compensatory responses that accelerate vascular remodeling.
- A self-reinforcing cycle of 'vascular-organ interactive injury' is established.
Conclusions:
- Arteriosclerosis leads to multi-organ damage through direct and indirect pathways.
- Dysfunction in cardiac, cerebral, and renal systems exacerbates arteriosclerosis.
- Current strategies for clinical assessment and intervention are outlined.
Abstract:
Arteriosclerosis is a systemic degenerative vascular disorder characterized by arterial wall thickening, reduced elasticity (arterial stiffness), and luminal narrowing, and is closely associated with aging and hypertension. Key pathological processes include lipid deposition, chronic inflammation, vascular calcification, and hemodynamic disturbances. These processes progressively injure high metabolic demand organs, including the heart, brain, and kidneys, through both direct vascular damage and indirect regulatory pathways. Conversely, injury to these target organs can activate compensatory and stress responses that further accelerate vascular remodeling, establishing a self-reinforcing cycle of "vascular-organ interactive injury." This review summarizes mechanisms by which arteriosclerosis drives multi-organ damage, highlights related clinical manifestations and outcomes, discusses how cardiac, cerebral, and renal dysfunction feeds back to worsening vascular disease, and outlines current strategies for clinical assessment and intervention.
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