Vascular calcification: Molecular mechanisms and therapeutic interventions

Area of Science:

• Cardiovascular Biology
• Pathology
• Molecular Medicine

Background:

• Vascular calcification (VC) is a pathological disorder linked to atherosclerosis, hypertension, and chronic kidney disease, posing significant health risks.
• While VC involves vascular smooth muscle cell transdifferentiation, mineral balance, and matrix vesicles, its precise molecular mechanisms require further elucidation.
• Emerging evidence indicates VC is an active, regulated process, not merely a passive comorbidity, suggesting potential for therapeutic intervention.

Purpose of the Study:

• To review novel findings on the molecular mechanisms underlying vascular calcification.
• To summarize recent therapeutic interventions targeting VC progression.
• To discuss controversial clinical approaches for managing VC.

Main Methods:

• Comprehensive literature review of studies on vascular calcification mechanisms.
• Analysis of research on inflammatory responses, cellular stress, and metabolic factors in VC.
• Evaluation of clinical evidence for various therapeutic agents and ion conditioning.

Main Results:

• VC progression is influenced by inflammatory responses, endoplasmic reticulum stress, mitochondrial dysfunction, iron homeostasis, and metabolic imbalances.
• Specific signaling pathways play crucial roles in the development of VC.
• Several therapeutic strategies targeting molecular mechanisms show promise, though clinical interventions remain debated.

Conclusions:

• Vascular calcification is a complex, active process with identifiable molecular drivers.
• Targeting these molecular pathways presents promising therapeutic avenues for VC.
• Further research is needed to clarify the efficacy and optimal use of interventions in clinical practice.