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<p>Circulating Growth Differentiation Factors 11 and 8 (GDF11/8) exist in both latent and active forms, and it is unclear if specific forms can predict disease outcomes. Our data suggest that a dual-specific aptamer selectively binds GDF11/8 after prodomain activation. In 11,609 patients at risk for future cardiovascular events, low dual-specific aptamer-detected GDF11/8 levels strongly predicted adverse outcomes, including cardiovascular events (HR = 0.43, <i>p</i> = 9.1 × 10⁻⁶³) and all-cause mortality (HR = 0.33, <i>p</i> = 4.8 × 10⁻⁴⁰). Use of selective aptamers suggested that results observed with the dual-specific aptamer for cardiovascular and mortality risk replicated with a GDF8 aptamer although with a smaller effect size. In a second cohort of 4110 individuals (ARIC), low dual-specific aptamer-detected GDF11/8 levels also predicted increased 8 year dementia risk (HR = 0.66, <i>p</i> = 0.00148). Our findings reveal that activation of GDF11/8 may be a factor in future aging-related cardiovascular and cognitive decline.</p>

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Activated GDF11/8 subforms predict cardiovascular events and mortality in humans

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月15日

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  • Ryan G. Walker,
  • Tomohiro Kato,
  • Laura Ben Driss,
  • Stephen A. Williams,
  • Michael A. Hinterberg,
  • Nebojsa Janjic,
  • Amy D. Gelinas,
  • Meredith A. Carpenter,
  • Chandramohan Kattamuri,
  • Joan E. Walter,
  • Christian Mueller,
  • Kourtney R. Mendello,
  • Justis V. Gordon,
  • Keenan A. Walker,
  • Josef Coresh,
  • Shalender Bhasin,
  • Lee L. Rubin,
  • Amy J. Wagers,
  • Thomas B. Thompson,
  • Peter Ganz,
  • Richard T. Lee

摘要

Circulating Growth Differentiation Factors 11 and 8 (GDF11/8) exist in both latent and active forms, and it is unclear if specific forms can predict disease outcomes. Our data suggest that a dual-specific aptamer selectively binds GDF11/8 after prodomain activation. In 11,609 patients at risk for future cardiovascular events, low dual-specific aptamer-detected GDF11/8 levels strongly predicted adverse outcomes, including cardiovascular events (HR = 0.43, p = 9.1 × 10⁻⁶³) and all-cause mortality (HR = 0.33, p = 4.8 × 10⁻⁴⁰). Use of selective aptamers suggested that results observed with the dual-specific aptamer for cardiovascular and mortality risk replicated with a GDF8 aptamer although with a smaller effect size. In a second cohort of 4110 individuals (ARIC), low dual-specific aptamer-detected GDF11/8 levels also predicted increased 8 year dementia risk (HR = 0.66, p = 0.00148). Our findings reveal that activation of GDF11/8 may be a factor in future aging-related cardiovascular and cognitive decline.