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Related Concept Videos

Functions of Smooth Muscles01:23

Functions of Smooth Muscles

3.4K
Smooth muscles are an important type of muscle tissue that plays a vital role in the involuntary movements of internal organs. For example, they help regulate the movement of food through the gut and the flow of blood through the circulatory system.
Function of visceral smooth muscles
Visceral smooth muscle is found in the walls of all hollow organs, except the heart, and is a key player in the involuntary movements that drive the functioning of these internal organs. This tissue is arranged in...
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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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Structure and Organization of Smooth Muscles01:13

Structure and Organization of Smooth Muscles

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Smooth muscle tissue is a type of muscle tissue that can be found lining various vital organs in the human body, including the lungs, blood vessels, digestive tract, and respiratory tract. This type of tissue is responsible for regulating the movements of these organs, playing crucial roles in the functioning of various systems, including the vascular, digestive, respiratory, and urinary systems.
Structure of smooth muscle cell
Smooth muscle cells are spindle-shaped with tapering ends and a...
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The Cell Cycle Control System01:28

The Cell Cycle Control System

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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and...
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The Cell Cycle Control System02:11

The Cell Cycle Control System

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The cell cycle is an organized set of events that leads the cell to divide into two daughter cells, each containing chromosomes identical to the parent cell. It is the cell cycle that leads to the formation of an entire organism from a single-cell zygote. Besides, cell division also functions in the renewal or repair of tissues in adult multicellular eukaryotes. For example, in the bone marrow, the stem cells divide to form new blood cells. Although essential for several functions, cell...
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The Role of Actin and Myosin in Non-muscle Cells01:10

The Role of Actin and Myosin in Non-muscle Cells

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Actin and myosin or actomyosin filaments also play a significant role in cells other than those involved in muscle contraction (which occurs within the sarcomere of muscle cells). The mechanism of non-muscle cell contractile bundles was first observed in Dictyostelium and Acanthamoeba. In non-muscle cells, two bundles are commonly found: stress fibers and actomyosin adherence belts. These contractile bundles are smaller and less organized than the ones found in muscle cells. They  are held...
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Updated: Feb 6, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

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Single-Cell Multimodal Profiling Highlights Persistent Aortic Smooth Muscle Cell Changes in Diabetic Mice Despite

Vinay Singh Tanwar1, Vajir Malek1, Jingyi Wang2

  • 1Department of Diabetes Complications and Metabolism, Arthur Riggs Diabetes and Metabolism Research Institute (V.S.T., V.M., Y.L., N.K.M., M.A., L.L., M.A.R., Z.B.C., R.N.), Beckman Research Institute of City of Hope, Duarte, CA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|February 5, 2026
PubMed
Summary
This summary is machine-generated.

Type 2 diabetes causes vascular smooth muscle cell (SMC) dysfunction that persists despite glucose control. A drug did not reverse these diabetic changes, highlighting the need for new therapies targeting metabolic memory.

Keywords:
aortacardiovascular diseasesdiabetes mellitus, type 2epigenomicsglycemic controlmultiomicssodium-glucose transporter 2 inhibitors

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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Diseases
  • Epigenetics

Background:

  • Type 2 diabetes accelerates vascular complications like hypertension and atherosclerosis.
  • Vascular smooth muscle cell (SMC) phenotypic switching is a key driver of these complications and is enhanced in diabetes.
  • SMC dysfunction can persist despite glycemic control due to prior hyperglycemia (metabolic memory).

Purpose of the Study:

  • To investigate the transcriptomic and epigenomic changes in SMCs during phenotypic transition in type 2 diabetes.
  • To examine the effect of glucose normalization on these changes using single-cell multiomics.

Main Methods:

  • Type 2 diabetes mice (db/db) were treated with dapagliflozin (DAPA) or vehicle; control mice (db/+) received vehicle.
  • Aortas were analyzed using single-cell RNA sequencing, single-cell assay for transposase-accessible chromatin with sequencing, and spatial transcriptomics.
  • SMC subtypes, gene expression, chromatin accessibility, and transcription factor activity were assessed.

Main Results:

  • Dapagliflozin effectively controlled blood glucose and HbA1c in diabetic mice.
  • Diabetes induced decreased SMC contractile pathways and increased fibrosis, inflammation, and endothelial dysfunction markers.
  • These diabetes-associated changes in gene expression were only partly reversed by DAPA, while chromatin accessibility changes were not reversed.
  • SMC phenotypic transition from contractile to fibromyocyte-like states was associated with increased transcription factor activity.

Conclusions:

  • Type 2 diabetes induces significant gene expression and chromatin accessibility changes in aortic SMCs, promoting phenotypic switching.
  • These molecular alterations are not effectively reversed by dapagliflozin, indicating limitations in current therapies.
  • Novel therapeutic strategies are needed to address the persistent SMC dysfunction driven by the metabolic memory of hyperglycemia.