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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Hematology

Background:

  • Aging and chronic inflammation are independent risk factors for atherothrombosis and cardiovascular disease.
  • Platelet hyperreactivity and increased thrombotic risk are observed during aging.

Purpose of the Study:

  • To investigate the role of aging-associated inflammation in promoting platelet hyperreactivity and thrombotic risk.
  • To identify the specific inflammatory mediators involved and their mechanisms of action.

Main Methods:

  • Functional platelet studies in aged-frail adults and old mice.
  • In vivo studies using a mouse model of aging with TNF-α receptor blockade.
  • Analysis of bone marrow compartments and megakaryocyte progenitor cells.
  • Single-cell RNA-sequencing and metabolomics of mouse platelets.
  • Comparison with platelets from patients with myeloproliferative neoplasms.

Main Results:

  • Aged platelets exhibit hyperreactivity and form larger thrombi.
  • Tumor necrosis factor alpha (TNF-α) is identified as the key pro-inflammatory cytokine driving platelet hyperreactivity.
  • Abrogating TNF-α receptor signaling in vivo neutralized platelet hyperreactivity.
  • Aging leads to platelet-biased hematopoiesis and megakaryocyte reprogramming.
  • TNF-α induces mitochondrial changes (increased mass, oxygen consumption) in platelets, which are reversible upon blockade.
  • Age-dependent metabolic profiles in platelets may influence activation.

Conclusions:

  • TNF-α critically regulates megakaryocytes in the bone marrow niche.
  • TNF-α is a key driver of aging-associated platelet hyperreactivity and thrombosis.
  • Targeting TNF-α signaling may offer a therapeutic strategy to mitigate age-related thrombotic risk.