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Eur J Clin Invest. 2026 Jan;56(1):e70133. doi: 10.1111/eci.70133. Epub 2025 Oct 3.

Autores:

Mark Atallah  1 , Nadim Nasrallah  1 , Tarek Harb  1 , Gary Gerstenblith  1 , Thorsten M Leucker  1

Conclusión: While environmental factors such as inflammation and hormonal status can transiently modulate levels, genetic variation overwhelmingly dictates lifelong Lp(a) burden. As novel agents targeting Lp(a) enter late-stage clinical trials, mechanistic insights into Lp(a) biology will be essential to risk stratification and future clinical management.

Conclusion: There are no currently approved lipid-lowering therapies that substantially reduce Lp(a) levels. Novel agents to lower Lp(a) include antisense oligonucleotides, small interfering ribonucleic acid and small molecules, all of which have shown promising results in phase 2 trials. Ongoing phase 3 trials will evaluate the causal relationship between Lp(a) and ASCVD, and whether lowering Lp(a) reduces cardiovascular outcomes.

Eur J Clin Invest. 2026 Jan;56(1):e70127. doi: 10.1111/eci.70127. Epub 2025 Oct 3.

Autores:

Nadim Nasrallah  1 , Mark Atallah  1 , Tarek Harb  1 , Gary Gerstenblith  1 , Thorsten M Leucker  1

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