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Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

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Related Experiment Video

Updated: May 14, 2026

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
09:53

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

MicroRNA-34a regulates cardiac ageing and function.

Reinier A Boon1, Kazuma Iekushi, Stefanie Lechner

  • 1Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University Frankfurt, 60590 Frankfurt, Germany.

Nature
|February 22, 2013
PubMed
Summary

Ageing hearts show increased microRNA-34a (miR-34a), causing cell death and dysfunction. Inhibiting miR-34a protects the aging heart and improves recovery after heart attacks by targeting PNUTS.

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Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
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Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization

Published on: September 15, 2018

Related Experiment Videos

Last Updated: May 14, 2026

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
09:53

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
08:22

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization

Published on: September 15, 2018

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Cardiology

Background:

  • Aging is the primary risk factor for cardiovascular diseases, worsening outcomes in acute myocardial infarction.
  • MicroRNAs (miRNAs) are key regulators of cardiovascular function and aging.
  • Altered cardiac miRNA expression during aging contributes to functional decline.

Purpose of the Study:

  • To investigate the role of altered miRNA expression in age-dependent cardiac dysfunction.
  • To determine the specific contribution of miR-34a to cardiac aging and response to myocardial infarction.

Main Methods:

  • Analysis of miRNA expression in aging hearts.
  • In vivo silencing and genetic deletion of miR-34a.
  • Assessment of cardiomyocyte cell death, fibrosis, and cardiac function post-myocardial infarction.
  • Identification of direct miRNA targets using molecular assays.

Main Results:

  • miR-34a is induced in the aging heart.
  • Inhibition or deletion of miR-34a reduces age-associated cardiomyocyte death.
  • miR-34a inhibition improves cardiac function and reduces fibrosis after myocardial infarction.
  • PNUTS was identified as a direct miR-34a target, mediating effects on telomere length and DNA damage.

Conclusions:

  • Age-induced miR-34a contributes to cardiac aging and poor outcomes after myocardial infarction.
  • Targeting miR-34a and its downstream effector PNUTS offers a therapeutic strategy for age-related cardiovascular conditions.