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Peer-reviewedCC BY 4.0Cardiovascular Therapeutics

PCSK9 and Atrial Fibrillation: A New Perspective on an Old Problem

  • Amirhossein Sahebkar1,2,3
  • Wael Almahmeed4
  • Prashant Kesharwani5,6
  • Tannaz Jamialahmadi7
7 affiliations
  1. 1Biotechnology Research Center Pharmaceutical Technology Institute School of Pharmacy Mashhad University of Medical Sciences Mashhad Iran mums.ac.ir
  2. 2Centre for Research Impact & Outcome Chitkara College of Pharmacy Chitkara University Rajpura Punjab India chitkara.edu.in
  3. 3Applied Biomedical Research Center Basic Sciences Research Institute Mashhad University of Medical Sciences Mashhad Iran mums.ac.ir
  4. 4Heart and Vascular Institute Cleveland Clinic Abu Dhabi Abu Dhabi UAE clevelandclinicabudhabi.ae
  5. 5Next-Generation Translational Nanomedicine Laboratory Department of Pharmaceutical Sciences Dr. Harisingh Gour Vishwavidyalaya (A Central University) Sagar Madhya Pradesh India
  6. 6University Institute of Pharma Sciences Chandigarh University Mohali Punjab India chandigarhuniversity.ac.in
  7. 7Pharmaceutical Research Center Pharmaceutical Technology Institute School of Pharmacy Mashhad University of Medical Sciences Mashhad Iran mums.ac.ir
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Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel contributor to atrial fibrillation (AF) pathophysiology. Recent studies suggest that elevated PCSK9 levels may promote AF through multiple mechanisms, including platelet activation, oxidative stress, vascular calcification, and structural atrial remodeling. PCSK9 inhibitors such as alirocumab, evolocumab, and newer agents like inclisiran have shown potential in reducing AF incidence and cardiovascular events, particularly in high‐risk populations. However, evidence from randomized controlled trials with AF as a primary clinical endpoint is limited. Further mechanistic and interventional research is warranted to establish optimized therapeutic strategies targeting PCSK9 in AF prevention and management.

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Cite

BibTeXRIS
BibTeX
@article{sahebkar2026pcsk9,
  title = {{PCSK9 and Atrial Fibrillation: A New Perspective on an Old Problem}},
  author = {Amirhossein Sahebkar and Wael Almahmeed and Prashant Kesharwani and Tannaz Jamialahmadi},
  journal = {Cardiovascular Therapeutics},
  year = {2026},
  month = oct,
  doi = {10.1155/cdr/7328020},
  url = {https://doi.org/10.1155/cdr/7328020},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - PCSK9 and Atrial Fibrillation: A New Perspective on an Old Problem
AU  - Amirhossein Sahebkar
AU  - Wael Almahmeed
AU  - Prashant Kesharwani
AU  - Tannaz Jamialahmadi
PY  - 2026
DA  - 2026/10/26
JO  - Cardiovascular Therapeutics
DO  - 10.1155/cdr/7328020
UR  - https://doi.org/10.1155/cdr/7328020
AB  - Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel contributor to atrial fibrillation (AF) pathophysiology. Recent studies suggest that elevated PCSK9 levels may promote AF through multiple mechanisms, including platelet activation, oxidative stress, vascular calcification, and structural atrial remodeling. PCSK9 inhibitors such as alirocumab, evolocumab, and newer agents like inclisiran have shown potential in reducing AF incidence and cardiovascular events, particularly in high‐risk populations. However, evidence from randomized controlled trials with AF as a primary clinical endpoint is limited. Further mechanistic and interventional research is warranted to establish optimized therapeutic strategies targeting PCSK9 in AF prevention and management.
SN  - 1755-5914
SN  - 1755-5922
ER  -