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Related Concept Videos

Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Cellular Injury II: Classification01:21

Cellular Injury II: Classification

Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

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Related Experiment Video

Updated: Jun 26, 2026

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Cellular Stress and Molecular Responses in Bladder Ischemia.

Jing-Hua Yang1,2, Han-Pil Choi2, Wanting Niu3

  • 1Department of Surgery, Boston University School of Medicine, Boston, MA 02118, USA.

International Journal of Molecular Sciences
|November 13, 2021
PubMed
Summary

Bladder ischemia, linked to atherosclerosis, can cause urinary urgency or incontinence. Cellular stress responses are key to understanding and treating these lower urinary tract symptoms.

Keywords:
bladder ischemiacellular stressnon-coded amino acidspost-translational modifications

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Area of Science:

  • Urology
  • Cellular Biology
  • Vascular Biology

Background:

  • Bladder ischemia, resulting from pelvic arterial atherosclerosis, is increasingly recognized as a factor in lower urinary tract symptoms (LUTS).
  • Early ischemia can lead to detrusor overactivity, while severe, prolonged ischemia may cause detrusor underactivity.

Purpose of the Study:

  • To explore the cellular mechanisms underlying bladder ischemia's impact on detrusor function.
  • To identify molecular players involved in the bladder's response to ischemic conditions.

Main Methods:

  • Review of experimental models and clinical studies on bladder ischemia and LUTS.
  • Analysis of cellular energy and stress sensors, stress response molecules, and downstream pathways.

Main Results:

  • Adenosine monophosphate-activated protein kinase plays a role in detrusor overactivity and neurodegeneration.
  • Apoptosis signal-regulating kinase 1, caspase-3, and heat shock proteins contribute to smooth muscle changes and apoptosis.
  • Hypoxia-inducible factor, TGF-beta, VEGF, and NGF are implicated downstream pathways.

Conclusions:

  • Cellular energy and stress responses are central to bladder dysfunction in ischemia.
  • Molecular alterations include differential protein expression and modified contractile proteins.
  • Understanding these cellular responses may reveal new diagnostic and therapeutic targets for LUTS.