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  1. Home
  3. Lumican Is Both A Novel Risk Factor And Potential Plasma Biomarker For Vascular Aging, Capable Of Promoting Vascular Smooth Cells Senescence Through Interacting With Integrin Α2β1.
  1. Home
  3. Lumican Is Both A Novel Risk Factor And Potential Plasma Biomarker For Vascular Aging, Capable Of Promoting Vascular Smooth Cells Senescence Through Interacting With Integrin Α2β1.

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Lumican Is Both a Novel Risk Factor and Potential Plasma Biomarker for Vascular Aging, Capable of Promoting Vascular

Mandi Luo1,2, Dan Yan1,2, Yi Huang1,2

  • 1Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|August 27, 2024

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
LUMPulse wave velocitySynthetic phenotypeVSMCsVascular aging

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Lumican (LUM) is elevated in vascular aging and promotes arterial stiffening by interacting with integrin α2β1. Reducing LUM levels may offer a new therapeutic strategy for age-related vascular diseases.

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Medicine

Background:

  • Vascular aging contributes to chronic diseases in older adults, but its mechanisms are not fully understood.
  • Lumican (LUM) and integrin α2β1 are implicated in fibrosis and cell regulation, yet their roles in vascular aging are unclear.

Purpose of the Study:

  • To investigate the association between Lumican (LUM) and vascular aging.
  • To elucidate the mechanism of LUM and integrin α2β1 in vascular aging.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were used to measure LUM levels.
  • Western blot analysis and angiotensin II-induced senescence models in mice and vascular smooth cells (VSMCs) were employed.
  • Integrin α2β1 antagonist treatment was performed in vitro.

Main Results:

  • Plasma LUM levels were elevated in individuals with vascular aging and correlated with arterial stiffness.
  • LUM was upregulated in aged arteries and senescent VSMCs.
  • LUM semiknockout mice showed reduced arteriosclerosis, hypertension, and vascular aging.
  • LUM deficiency suppressed senescence markers (p53, p21) and fibrosis (collagen 1, collagen 3) in VSMCs.
  • Integrin α2β1 antagonism reversed LUM-induced changes.

Conclusions:

  • Lumican (LUM) is a potential biomarker and risk factor for vascular aging.
  • LUM promotes vascular aging and pathological changes via the integrin α2β1 pathway in VSMCs.
  • Targeting LUM offers a novel therapeutic approach for vascular aging and related diseases.