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ADAM17 contributes to heart failure after heart attack by promoting loss of cardioprotective ACE2
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Myocardial infarction (MI), or heart attack, can cause long-term damage that leads to heart failure. To treat this type of heart failure, it’s critical to heal the pathological structural changes in the heart and preserve cardiac function. A recent study investigated potential treatment targets by exploring the role of the enzyme ADAM17, whose levels are increased during MI. In a group of 152 patients with MI, high ADAM17 levels were associated with a greater incidence of subsequent heart failure, as well as poorer heart function and higher mortality, suggesting a negative role of ADAM17. In mice with MI, elevated ADAM17 levels were linked to heart damage, but blocking ADAM17 activity limited the cardiac damage and remodeling after MI. Experiments in cultured heart cells revealed that ADAM17 exerted its harmful effects by promoting loss of the cardioprotective enzyme ACE2 and that the activation of ADAM17 depended on modification of a specific site in the protein p38 MAPK..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
04/17/2023
Biology
Unrestricted Use
CC BY
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Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

Subject:
Biology
Life Science
Material Type:
Full Course
Provider:
Rice University
Provider Set:
OpenStax College
Date Added:
08/22/2012
Biology, Animal Structure and Function, The Circulatory System, Mammalian Heart and Blood Vessels
Conditional Remix & Share Permitted
CC BY-NC-SA
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By the end of this section, you will be able to:Describe the structure of the heart and explain how cardiac muscle is different from other musclesDescribe the cardiac cycleExplain the structure of arteries, veins, and capillaries, and how blood flows through the body

Subject:
Applied Science
Biology
Life Science
Material Type:
Module
Author:
Tina B. Jones
Date Added:
07/24/2019
Biology, Animal Structure and Function, The Circulatory System, Mammalian Heart and Blood Vessels
Conditional Remix & Share Permitted
CC BY-NC
Rating
0.0 stars

By the end of this section, you will be able to:Describe the structure of the heart and explain how cardiac muscle is different from other musclesDescribe the cardiac cycleExplain the structure of arteries, veins, and capillaries, and how blood flows through the body

Subject:
Applied Science
Biology
Life Science
Material Type:
Module
Date Added:
07/10/2017
Clarifying the role of noncoding RNAs in cardiac fibrosis
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CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cardiac fibrosis, or scarring of heart tissue, is a common finding in many disorders of the heart, including myocardial infarction, hypertension, and cardiac hypertrophy. A key step in this form of scarring is the transformation of fibroblasts, cells that provide structural, electrical, and chemical support into myofibroblasts, more muscle-like cells expressed only in stressed or failing hearts. A new review explores the important role played by noncoding RNAs in this transformation. Noncoding RNAs, studies are showing, regulate fibrotic scarring through the TGF-β and WNT signaling pathways. TGF-β signaling participates in a variety of heart-related processes, including cardiac repair, hypertrophy, fibrotic remodeling, and fibroblast activation. WNT signaling, meanwhile, is implicated in the pathogenesis of many diseases. Crosstalk between the TGF-β and WNT pathways could be responsible for the transcription of genes that promote fibrosis..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
10/30/2020
A G protein and PDE enzymes help regulate adrenergic signaling for cardiac control
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CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The pumping action of the heart is tightly regulated by many factors. For example, the ion channel proteins RyR2 and SERCA2a regulate cardiac contraction via the β adrenergic receptor (βAR) pathway and under stress conditions, βAR stimulation promotes the enzyme activity of PKA to ultimately enhance cardiac contraction and relaxation. However, it’s unclear exactly how βAR-stimulated PKA dynamically affects RyR2 and SERCA2a within their nano-scale subcellular domains. To learn more, researchers recently used biosensors to detect PKA activity at these nanodomains in heart cells from mice, rats, and rabbits. They found that the βAR subtype β₁AR signaled to both RyR2 and SERCA2a nanodomains via PKA, while β₂AR did not. Specifically, β₂AR signaling at these nanodomains was prevented by the enzymes PDE3 and PDE4, which controlled baseline PKA activity, but blocking an inhibitory G protein permitted β₂AR signaling at the RyR2 nanodomains..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
04/14/2023
RGS4 promotes cardiac fibrosis in mice with heart attack
Unrestricted Use
CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cardiac fibrosis is tissue scarring that typically follows a heart attack. Growing evidence suggests that this scarring process is mediated by RGS proteins, multifunctional regulators of cell signaling. To better understand how, researchers examined the effects of RGS4, both on in vitro and in vivo models of heart attack. All models showed elevated levels of RGS4, linking the protein to cardiac fibrosis. Silencing RGS4 through RNA interference proved capable of reducing cardiac fibrosis in vitro and in mice. But when overexpressed, RGS4 could counteract the protective effects of choline, a nutrient found in meat that has been shown to reduce cardiac fibrosis. Further experiments revealed that RGS4 exerts its pro-cardiac fibrosis effects through TGFβ1/Smad and MAPK signaling. Future studies will examine how RGS4 interacts with similar proteins to cause cardiac fibrosis, which could lead to new ways of combating the harmful after-effects of heart attack..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
10/16/2021
Visualizing calcium “death waves” in heart cells
Unrestricted Use
CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cell death is a hallmark of various abnormalities of the heart, including heart failure, heart attack, and ischemia. While the long-term effects of cell death in the heart have been described, the cellular processes that occur immediately after cell death remain poorly understood. Now, by tracking the movement of calcium ions, researchers are gaining a better idea of what happens right after individual heart cells die. Calcium ions regulate vital cell functions in mammals and therefore serve as a valuable signal of cellular activity and intercell connections. When zapping and killing a single heart muscle cell with a laser, researchers found that different types of surrounding cells responded differently. Nearby myocytes showed a slow and sustained uptick in calcium “sparks,” while distant myocytes were weakly or not affected. This activity was accompanied by mechanical damage in myocytes. Fibroblasts, however, showed rapid shock waves of calcium ion activity..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider Set:
Video Bytes
Date Added:
02/25/2021