Articles tagged with Cell Apoptosis
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Cirrhotic cardiomyopathy involves structural, inflammatory, and metabolic pathologies. Inflammation and mitochondrial dysfunction promote cardiac damage, and the liver-heart axis highlights the impact of cirrhosis severity on cardiac health.
A study investigates dynamic changes in cardiac function and mitochondrial damage in a mouse model of cirrhotic cardiomyopathy. Key findings include progressive cardiac dysfunction, inflammation, and mitochondrial injury contributing to disease progression.
Researchers have discovered a complex regulatory circuit involving SRSF1, AURKA, and MYC that promotes aggressive pancreatic cancer progression. The circuit, which involves alternative splicing, can be targeted with an antisense oligonucleotide to reduce tumor cells' viability and trigger apoptosis.
Researchers developed a new approach using the microbial protein Archaerhodopsin-3 to induce apoptosis in cancer cells, leading to significant tumor shrinkage when exposed to green light. The findings, published by Okayama University, show great potential for this light-activated molecule as a novel cancer therapy.
Researchers identified C-C chemokine ligand 5 (CCL5) as a key player in kidney injury and repair, with the molecule behaving both protectively and harmfully. The study suggests future drugs could target only its damaging effects, paving the way for more precise treatments for chronic kidney disease.
Researchers explore ZBP1-mediated programmed cell death, its mechanisms, and therapeutic strategies for systemic diseases. The review also discusses ZBP1's involvement in various types of cell death, including apoptosis, necroptosis, pyroptosis, and ferroptosis.
BH3 mimetics demonstrate potent anti-cancer activity by targeting pro-survival BCL-2 proteins, effectively eradicating leukaemia cells with complex mutations. The review highlights several important findings about BH3 mimetics and their role in treating acute myeloid leukaemia.
A team of scientists has developed a protein-based therapeutic tool called Crunch to target and remove specific living cells, such as cancer cells or overactive immune cells. The new system uses the body's natural waste removal system to clear out unwanted cells, offering hope for improved treatments.
Researchers discovered that impaired autophagy causes abnormal accumulation of NR2F1 protein, which activates the STAT3 signaling pathway and triggers fibrosis, apoptosis, and cataract progression. Silencing NR2F1 in cells and mouse models suppressed these pathological features and reduced lens opacity.
Researchers have identified RG7388 as exhibiting promising antiviral activity against Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV), a tick-borne pathogen with a high mortality rate. The study found that RG7388 can inhibit virus replication by enhancing cells' sensitivity to apoptotic stimulation signals.
Research on MCL-1 protein reveals its critical role in cell survival and energy production, offering a roadmap for designing targeted cancer therapies with reduced side effects. The findings also shed light on fatal metabolic diseases in infants, providing potential new targets for future treatments.
A new study suggests that a drug used to prevent alcohol abuse can also interrupt runaway cell death and inflammation triggered by severe trauma, particularly in female mice. The findings may lead to therapies that could shorten hospital stays and improve survival rates if administered promptly after traumatic injuries.
Researchers identified miR-146b as a key regulator of beta-cell decline during obesity-to-T2DM progression. The study showed that miR-146b suppresses the expression of Btg2, leading to increased apoptosis and decreased insulin synthesis and secretion.
Adding an experimental cancer drug to standard TB treatment reduces lung damage and prevents post-TB lung disease in mice. Researchers found that the drug doubled pulmonary apoptosis and reduced lung scarring by 40% compared to standard treatments.
This study investigates TNIP1's role in regulating cell proliferation and apoptosis in breast cancer. TNIP1 knockdown was found to induce growth arrest and activate the NF-κB pathway, leading to increased apoptosis in breast cancer cells. The findings highlight TNIP1 as a crucial marker for breast cancer therapies.
Researchers have discovered Ferroptosis Suppressor Protein 1 (FSP1) plays a pivotal role in intervertebral disc degeneration, accelerating disc degeneration through caspase 3-dependent apoptosis and mitochondrial damage. Inhibiting FSP1 may offer relief to millions suffering from chronic back pain.
Researchers at Doshisha University reveal that 25-hydroxycholesterol causes a specific type of cell death called ferroptosis, which could contribute to various diseases. The study identifies two key mechanisms by which 25-OHC induces ferroptosis, including inhibition of cellular pathways and disruption of antioxidant systems.
Research finds ELK3 inhibits ferroptosis and proliferation of rheumatoid arthritis fibroblast-like synoviocytes, affecting their biological activity. ELK3's molecular mechanism involves regulating kelch-like ECH-associated protein 1.
A review of cell death and aging in cancer research reveals the significance of cellular senescence in promoting cancer growth. The study highlights the potential of various types of programmed cell death, such as necroptosis and pyroptosis, as therapeutic targets against senescent cells.
This study used a senescence-accelerated prone strain 8 (SAMP8) male mice model to observe the protective effects of acupuncture on different brain regions in Alzheimer's disease. Acupuncture treatment improved learning and memory abilities, as well as depression-like behavior, by reducing apoptosis and decreasing tau protein deposition.
Regular aerobic exercise has been shown to significantly reduce disease markers associated with Alzheimer's, protecting healthy brain cells and restoring balance in the aging brain. The study highlights the potential for aerobic exercise to serve as a cornerstone in preventive strategies for Alzheimer's.
A study published in Chinese Medical Journal explores the use of artificial intelligence to identify potential medications for treating glaucoma. Researchers used AI models to predict the effectiveness of small-molecule compounds targeting RIPK3, a key signaling molecule involved in programmed cell death.
Researchers from Osaka University found that Foxo3 mediates erroneous cell elimination during vertebrate development, ensuring precise development and cancer prevention. The study identified a specific pathway involving Foxo3, N-cadherin, and reactive oxygen species to eliminate unfit cells with abnormal Shh activity levels.
Researchers discovered a novel platinum complex that targets androgen receptor signaling, inhibiting cell growth and survival in prostate cancer cells. The complex, 5-H-Y, showed stronger cytotoxic effects than cisplatin with minimal toxicity, offering a promising approach to treating advanced prostate cancer.
Research found that intermittent fasting inhibits hair growth in mice by causing oxidative stress on stem cells. A clinical trial showed a similar effect in humans, with a 18% reduction in hair growth speed.
A recent study has identified Kif23 as a key regulator of embryonic brain development, highlighting its potential link to microcephaly. The research found that Kif23 is essential for neural progenitor cell proliferation and differentiation, with deficiency leading to decreased cell growth and increased apoptosis.
Researchers develop a method to remove copper from tumor cells, killing them. The nanofibers use copper-binding domains to grasp copper ions, disrupting cellular homeostasis and increasing oxidative stress.
Researchers at Osaka University uncovered the molecular details of how Drosophila fruit fly cells are removed during development, challenging the common assumption that clustered apoptosis poses a disadvantage to organisms. This study may help determine how abnormal cell death leads to congenital defects in humans.
A comprehensive study examining over 16,000 necropsy records from 292 vertebrate species found significant differences in cancer prevalence. Cancer rates increase with body size and cellular mutation rates but decrease with longer gestation periods.
Metabolic dysfunction-associated steatohepatitis (MASLD) exhibits persistent activation of the DNA damage response (DDR) and its primary transcription factor P53 even after dietary reversal. Elevated P53 levels correlate with hepatocyte ballooning, suggesting a link between DDR signaling and MASLD recurrence.
Researchers discovered a calcium-based mechanism that aids in disposing of dead cells, shedding light on how bodies protect themselves from injury and disease. The study found that calcium ion levels are essential for efficient removal of dying or apoptotic cells from epithelial tissues.
Researchers discover PG3 activates p21, PUMA, and DR5 in cancer cells through ATF4 and ISR, independent of p53. The study provides insights into a novel mechanism by which PG3 induces cell death.
Pyroptosis, a form of programmed cell death traditionally thought to be purely inflammatory, also plays a crucial role in promoting healing and tissue repair. Cells undergoing pyroptosis release beneficial molecules that encourage wound healing.
A study published in Nature Communications reveals a cellular signaling pathway that promotes heart cell survival. The Mst1-FoxO1-C/EBP-β interaction stimulates protective mechanisms in cardiac myocytes, potentially paving the way for new therapies.
Researchers at NYU Abu Dhabi have discovered that the tumor suppressor protein Par-4 can cause a unique type of cell death called ferroptosis in human glioblastoma cells, while sparing healthy cells. This new understanding has the potential to inform the development of novel treatments for various hard-to-treat cancers and neurodegener...
A novel inhibitor HVH-2930 targeting heat shock protein 90 (HSP90) demonstrates efficacy against drug-resistant breast cancer cells. It selectively downregulates HER2 signaling, crucial for breast cancer progression, without triggering the heat shock response.
The study found that programmed cell death is a prerequisite for sperm release in liverworts. MpMLO1 protein increases cytoplasmic Ca2+ levels and induces PCD, allowing sperm to enter the antheridial pore for fertilization.
Researchers found that miR-377 reduces MYC mRNA levels, leading to increased Bax and PTEN expression and decreased CDK4. This results in induced apoptosis, inhibited proliferation, and arrested cell cycle in prostate cancer cells.
Researchers investigated the biological repercussions of UV-C radiation exposure from readily available domestic lamps and found that even brief exposure can lead to irreversible alterations in skin cells and retinal cells. The study highlights the need to prioritize safe utilization of these lamps to prevent potential harm.
Human umbilical cord mesenchymal stem cells (hUC-MSCs) have been shown to alleviate acute liver failure by inhibiting hepatocyte apoptosis and regulating macrophage polarization. This study suggests that hUC-MSC-based cell therapy may serve as an alternative option for patients with liver failure.
Researchers found that BTF3L4 overexpression mediates APAP-induced liver injury by inducing inflammation and damaging mitochondrial function. Increased BTF3L4 expression is positively associated with liver injury and may serve as a biomarker.
Researchers developed novel therapeutic bispecific antibodies targeting IgM and B-cell surface antigens, which directly inhibited cell proliferation via cell-cycle arrest and apoptosis in vitro. These findings suggest that anti-IgM/B-cell surface antigen-binding specific antibodies are promising therapeutic agents for B-cell malignancies.
Researchers found that geraniol reduces oxidative stress and neuroinflammation-mediated cognitive impairment in a mouse aging model. Geraniol treatment improved spatial learning and memory by enhancing anti-oxidant and anti-inflammatory effects.
Researchers identify mitochondrial priming as a key driver of multi-drug resistance in relapsed acute myeloid leukemia. A new technique called dynamic BH3 profiling reveals anti-cancer drugs capable of overcoming resistance.
Researchers from Florida Atlantic University found that alpha-santalol, a compound in sandalwood oil, decreases cell proliferation and induces apoptosis to prevent prostate cancer development. The study showed a 53% increase in normal tissue area in treated mice, indicating protection against prostate cancer progression.
GFH009 inhibits tumor growth and induces apoptosis in various HHM-derived cell lines. The compound's mechanism of action involves rapid 'on-off' inhibition of CDK9, which exerts a proapoptotic effect on cancer cells.
Researchers from Osaka University and University of Hawaii found that environmental microorganisms boost fruit fly reproduction by modifying hormone levels and increasing the production of germline stem cells. This discovery could lead to new avenues for improving reproductive health and fertility treatments.
Researchers found that BCMA-positive extracellular vesicles (EVs) in plasma levels correlated with myeloma patient responses to belantamab-mafodotin therapy. High EV levels preceded FLC progression and were associated with mafodotin-induced eryptosis.
Researchers found that FAAH inhibition reduced breast cancer growth in immunodeficient mice and induced apoptosis of breast cancer cells. The combination of FAAH inhibitors and endocannabinoids was the most effective treatment approach.
The Ghose lab will use the new SRM to study programmed cell death in tiny embryonic cells of the roundworm C. elegans. This technology will allow for finer detail and pinpoint documentation of cell death, advancing research on cell biology.
Researchers found that apoptotic cells induce apoptosis in neighboring hair follicle cells during the regression cycle. The study proposes a mathematical model of the hair follicle regression cycle, which suggests that the dermal papilla plays an essential role in initiating apoptosis.
Researchers discovered BMAL1 is significantly upregulated in senescent cells and modulates the senescence program through AP-1. The study highlights a previously unappreciated role of BMAL1 in regulating cellular senescence and circadian clock components.
A recent study found that apoptotic factors in eukaryotes have a bacterial or mitochondrial origin, suggesting conservation over 1.8 billion years. The researchers proposed an alternative scenario where early protoeukaryotes domesticated bacteria to produce toxins, which eventually evolved into apoptotic factors.
Mayo Clinic researchers found that cells expressing PD-1 and PD-L1 within a certain distance of each other can predict the success of immunotherapy in patients with colorectal cancer. This spatial analysis may help select patients most likely to benefit from treatment, improving outcomes and minimizing unnecessary treatments.
Autophagy helps protect cardiomyocytes from damage caused by anthracycline drugs like Doxorubicin. The study found that a protein regulator called ER-phagy alleviates Dox-induced cardiomyopathy, promoting cell survival.
Researchers discovered that Nerofe and Doxorubicin can downregulate KRAS signaling, leading to enhanced apoptosis in colorectal cancer cells. The combination also activates the immune system against tumor cells, increasing immunostimulatory cytokines and recruiting NK cells and M1 macrophages.
Researchers investigate MCL-1i-induced Mcl-1 protein accumulation and its implications in B-cell malignancies. The study reveals a complex mechanism contributing to MCL-1 protein stability upon treatment with MCL-1 inhibitors.
Researchers characterize a unique molecular mechanism in early stages of programmed cell death (apoptosis), a crucial process preventing cancer. By studying Bax protein interactions with mitochondrial lipids, they found that pore creation drives apoptosis initiation.
Researchers discovered that FDA-approved HDAC-inhibitors can impact energy metabolism in solid tumor cells, including glioblastoma. The combination of HDAC-inhibitors and imipridones may synergize to enhance killing of GBM cells by reversing cellular respiration.
Researchers have identified ATAD3A as a molecular determinant that favors the development of head and neck cancer. The protein is involved in various cellular processes, including energy metabolism and apoptosis. Targeting ATAD3A could offer a novel approach to developing effective anti-cancer therapeutics.