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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Related Experiment Video

Updated: Jun 2, 2025

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
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Elucidating emerging signaling pathways driving endothelial dysfunction in cardiovascular aging.

Anna De Bartolo1, Tommaso Angelone2, Carmine Rocca2

  • 1Cellular and Molecular Cardiovascular Physiology and Pathophysiology Laboratory, Department of Biology, E. and E. S. (DiBEST), University of Calabria, Arcavacata di Rende, Cosenza, Italy.

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Cardiovascular disease risk rises with age due to vascular aging, driven by inflammation and oxidative stress. Understanding these molecular pathways offers new therapeutic targets for heart health.

Keywords:
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Area of Science:

  • Cardiovascular biology
  • Gerontology
  • Molecular medicine

Background:

  • Cardiovascular diseases (CVD) risk significantly increases in older adults.
  • Aging vasculature contributes to CVD morbidity and mortality by disrupting endothelial balance.
  • Impaired vascular function and pathological remodeling are hallmarks of aging vasculature.

Purpose of the Study:

  • To review the impact of molecular pathways on cardiovascular aging.
  • To explore the interplay of inflammation, oxidative stress, and mitochondrial dysfunction in vascular aging.
  • To discuss the role of cellular senescence and cell-cell interactions in atherosclerosis progression.

Main Methods:

  • Review of key and emerging molecular pathways.
  • Focus on inflammatory signals (inflammaging), oxidative stress, and mitochondrial dysfunction.
  • Analysis of senescent cells and vascular-myeloid cell interactions.

Main Results:

  • Aging vasculature shows disrupted endothelial balance, impaired function, and pathological remodeling.
  • Chronic inflammation, oxidative stress, and mitochondrial dysfunction create a vicious cycle in cardiovascular aging.
  • Senescent endothelial and smooth muscle cells, along with vascular-myeloid cell interactions, impair plaque stability and promote atherosclerosis.

Conclusions:

  • Aberrant molecular pathways drive progressive vascular alterations during aging.
  • Cellular senescence and altered cell communication are critical in atherosclerosis.
  • Targeting these aging-related processes may offer therapeutic benefits for CVD.