ReviewAnnals of biomedical engineering2021
Mechanical Regulation of Apoptosis in the Cardiovascular System.
Review in Annals of biomedical engineering, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Cyclic stretch inhibits cell invasion in 3D scaffolds.bioRxiv : the preprint server for biology · 2026Article
- Focused ultrasound for cellular mechanoactivation and nanomedicine delivery in cancer.Biomedical microdevices · 2026Review
- Scaling-Up Vertical-Wheel Bioreactors Based on Cell Aggregate Exposure to Shear Stress and Energy Dissipation Rate.Annals of biomedical engineering · 2026Article
- Article
- Review
- Mechanosensing of Shear Stress and Uterine Spiral Artery Remodeling by Invasive Trophoblasts in Early Pregnancy.International journal of molecular sciences · 2025Review
- Theaflavin-3,3'-digallate protects against myocardial ischemia/reperfusion injury and hypoxia/reoxygenation injury by activating the PI3K/Akt/mTOR pathway.Journal of molecular histology · 2025Article
- CIRBP Enhances the Function of Yak Cumulus Cells by Activating AMPK/mTOR-Mediated Mitophagy.Biomolecules · 2025Article
- Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction.Current issues in molecular biology · 2024Review
- Gut matters in microgravity: potential link of gut microbiota and its metabolites to cardiovascular and musculoskeletal well-being.Nutrition & metabolism · 2024Review
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- Effects of gas signaling molecule SOThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Apoptotic vesicle-mediated senolytics requires mechanical loading.Theranostics · 2024Article
- Competition between deformation and free volume quantified by 3D image analysis of red blood cell.Biophysical journal · 2023Article
- Activation of PI3K/Akt mediates the protective effect of diallyl trisulfide on doxorubicin induced cardiac apoptosis.Current research in toxicology · 2023Article
- Aggregation-Induced Emission Luminogens for Cell Death Research.ACS bio & med chem Au · 2022Review
- Understanding Necroptosis in Pancreatic Diseases.Biomolecules · 2022Review
- L-Borneol 7-O-[Journal of immunology research · 2022Article
- Therapeutic potential of paeoniflorin in atherosclerosis: A cellular action and mechanism-based perspective.Frontiers in immunology · 2022Review
- Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target.International journal of biological sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis is a highly conserved physiological process of programmed cell death which is critical for proper organism development, tissue maintenance, and overall organism homeostasis. Proper regulation of cell removal is crucial, as both excessive and reduced apoptotic rates can lead to the onset of a variety of diseases. Apoptosis can be induced in cells in response to biochemical, electrical, and mechanical stimuli. Here, we review literature on specific mechanical stimuli that regulate apoptosis and the current understanding of how mechanotransduction plays a role in apoptotic signaling. We focus on how insufficient or excessive mechanical forces may induce apoptosis in the cardiovascular system and thus contribute to cardiovascular disease. Although studies have demonstrated that a broad range of mechanical stimuli initiate and/or potentiate apoptosis, they are predominantly correlative, and no mechanisms have been established. In this review, we attempt to establish a unifying mechanism for how various mechanical stimuli initiate a single cellular response, i.e. apoptosis. We hypothesize that the cytoskeleton plays a central role in this process as it does in determining myriad cell behaviors in response to mechanical inputs. We also describe potential approaches of using mechanomedicines to treat various diseases by altering apoptotic rates in specific cells. The goal of this review is to summarize the current state of the mechanobiology field and suggest potential avenues where future research can explore.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.