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Related Concept Videos

Smooth Muscle Contraction01:25

Smooth Muscle Contraction

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Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
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Mitochondrial Membranes01:45

Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondria01:37

Mitochondria

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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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The Inner Mitochondrial Membrane01:28

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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
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Related Experiment Video

Updated: Jul 10, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
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Mitochondrial influences on smooth muscle phenotype.

William J Pearce1

  • 1Department of Basic Sciences, Lawrence D. Longo, MD Center for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, California, United States.

American Journal of Physiology. Cell Physiology
|November 27, 2023
PubMed
Summary

Mitochondria play a crucial role in regulating smooth muscle cell phenotype. Disruptions in mitochondrial function, through mechanisms like mitophagy and fission, can lead to loss of vascular contractility.

Keywords:
metabolic reprogrammingmitoMirsmitochondria-associated membranesmitochondrial calciummitochondrial retrograde signaling

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Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Vascular Biology

Background:

  • Smooth muscle cells (SMCs) exhibit phenotypic plasticity, switching between contractile and noncontractile states.
  • Mitochondria significantly influence SMC phenotype through various signaling pathways and metabolic regulation.
  • Vascular pathologies often involve mitochondrial dysfunction, leading to altered SMC behavior.

Purpose of the Study:

  • To elucidate the multifaceted roles of mitochondria in regulating smooth muscle cell differentiation and phenotype.
  • To identify key mitochondrial molecules and processes that promote or inhibit SMC contractility.
  • To understand how mitochondrial dysfunction contributes to vascular diseases.

Main Methods:

  • Review of existing literature on mitochondrial function and smooth muscle cell biology.
  • Analysis of molecular pathways involving mitochondrial proteins, miRNAs, and metabolic reprogramming.
  • Examination of mitochondrial roles in calcium handling and intercellular communication.

Main Results:

  • Mitochondrial factors like prohibitin-2 promote contractility, while mitochondrial reactive oxygen species (mtROS) and high lactate inhibit it.
  • Mitophagy and mitochondrial fission are implicated in the loss of vascular contractility seen in diseases like pulmonary hypertension and atherosclerosis.
  • Mitochondria influence SMC phenotype via calcium signaling, retrograde signaling, and exosome secretion.

Conclusions:

  • Mitochondria are central regulators of smooth muscle cell phenotype and differentiation.
  • Mitochondrial dysfunction is a key driver of smooth muscle cell abnormalities in vascular pathologies.
  • Targeting mitochondrial pathways may offer therapeutic strategies for vascular diseases.