Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication DOI Creative Commons
Majeed M. A. Ali

Egyptian Liver Journal, Journal Year: 2024, Volume and Issue: 14(1)

Published: Nov. 12, 2024

Abstract Background Polyploidization, a process where cells acquire additional chromosome sets, is unique characteristic of hepatocytes. This has been increasingly recognized as an adaptive mechanism for maintaining liver function during aging, period characterized by cellular senescence, DNA damage, and metabolic dysregulation. Purpose review explores the molecular mechanisms underlying hepatocyte polyploidization its potential role in promoting resilience against aging-related decline function. We assess how polyploid hepatocytes contribute to genomic stability, stress resistance, adaptation, highlighting their relevance aging. Main body Hepatocyte occurs through such cytokinesis failure endoreplication, leading binuclear or mononuclear cells. Polyploid exhibit enhanced repair capacity, which helps mitigate accumulation age-related damage. The increased gene dosage facilitates better responses, particularly oxidative genotoxic insults. Metabolic adaptations, including xenobiotic metabolism lipid regulation, further support liver’s ability maintain homeostasis Additionally, demonstrate altered epigenetic landscapes proteostasis mechanisms, contributing improved reduced susceptibility senescence. These adaptations collectively enhance structural challenges. Conclusion represents critical protective that safeguard instability, dysfunction, stress. Understanding pathways driving could pave way novel therapeutic strategies combat disorders health span. Graphical

Language: Английский

Autophagy and the unfolded protein response shape the non-alcoholic fatty liver landscape: decoding the labyrinth DOI
Zahra Dashti, Zeynab Yousefi,

Pouria Kiani

et al.

Metabolism, Journal Year: 2024, Volume and Issue: 154, P. 155811 - 155811

Published: Feb. 2, 2024

Language: Английский

Citations

19
Association of dietary inflammatory potential, dietary oxidative balance score and biological aging DOI
Xuanyang Wang,

S Sarker,

Licheng Cheng

et al.

Clinical Nutrition, Journal Year: 2023, Volume and Issue: 43(1), P. 1 - 10

Published: Nov. 15, 2023

Language: Английский

Citations

26
Cellular senescence and wound healing in aged and diabetic skin DOI Creative Commons
Arisa Kita, Sena Yamamoto, Yuki Saito

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 19, 2024

Cellular senescence is a biological mechanism that prevents abnormal cell proliferation during tissue repair, and it often accompanied by the secretion of various factors, such as cytokines chemokines, known senescence-associated secretory phenotype (SASP). SASP-mediated cell-to-cell communication promotes regeneration, development. However, senescent cells can accumulate abnormally at injury sites, leading to excessive inflammation, dysfunction, intractable wounds. The effects cellular on skin wound healing be both beneficial detrimental, depending condition. Here, we reviewed functional differences in emerge healing, chronic aging. We also review latest mechanisms epidermis, dermis, subcutaneous fat, with focus senescence, regeneration. Finally, discuss potential clinical applications promoting inhibiting maximize benefits minimize detrimental effects.

Language: Английский

Citations

13
ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation DOI Creative Commons
Li Yang, J. Q. You, Xincheng Yang

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: Feb. 28, 2025

Senescence-associated secretory phenotype (SASP) mediates the biological effects of senescent cells on tissue microenvironment and contributes to ageing-associated disease progression. ACSS2 produces acetyl-CoA from acetate epigenetically controls gene expression through histone acetylation under various circumstances. However, whether how regulates cellular senescence remains unclear. Here, we show that pharmacological inhibition deletion Acss2 in mice blunts SASP abrogates pro-tumorigenic immune surveillance functions cells. Mechanistically, directly interacts with promotes PAICS, a key enzyme for purine biosynthesis. The PAICS autophagy-mediated degradation limit metabolism reduces dNTP pools DNA repair, exacerbating cytoplasmic chromatin fragment accumulation SASP. Altogether, our work links ACSS2-mediated local generation dictates functionality SASP, identifies as potential senomorphic target prevent senescence-associated diseases. Through producing acetate, expression. authors link ACSS2-generated CCF-SASP.

Language: Английский

Citations

1
Autophagy and Senescence: The Molecular Mechanisms and Implications in Liver Diseases DOI Open Access

Li Qiao,

Yan Lin,

Guangyu Liang

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(23), P. 16880 - 16880

Published: Nov. 28, 2023

The liver is the primary organ accountable for complex physiological functions, including lipid metabolism, toxic chemical degradation, bile acid synthesis, and glucose metabolism. Liver function homeostasis essential stability of bodily functions involved in regulation balance between cell proliferation death. Cell proliferation-halting mechanisms, autophagy senescence, are implicated development several diseases, such as cholestasis, viral hepatitis, nonalcoholic fatty disease, fibrosis, hepatocellular carcinoma. Among various death a highly conserved self-degradative cellular process that recycles damaged organelles, debris, proteins. This also provides substrate further A defect machinery can lead to premature accelerated aging, inflammatory state, tumorigenesis, senescence. Senescence, another type, an active player eliminating premalignant cells. At same time, senescent cells affect neighboring by secreting senescence-associated secretory phenotype induce paracrine Autophagy promote delay senescence under different contexts. review decodes roles multiple diseases achieve better understanding regulatory mechanisms implications diseases.

Language: Английский

Citations

19
Immune surveillance of senescence: potential application to age-related diseases DOI

Teh‐Wei Wang,

Makoto Nakanishi

Trends in Cell Biology, Journal Year: 2024, Volume and Issue: unknown

Published: July 1, 2024

Language: Английский

Citations

8
mTORC1 in energy expenditure: consequences for obesity DOI
C. Allard, Cristina Miralpeix, Antonio J. López-Gambero

et al.

Nature Reviews Endocrinology, Journal Year: 2024, Volume and Issue: 20(4), P. 239 - 251

Published: Jan. 15, 2024

Language: Английский

Citations

7
Association between fatigue, peripheral serotonin, and L-carnitine in hypothyroidism and in chronic fatigue syndrome DOI Creative Commons

Tommi Raij,

K. Raij

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: March 5, 2024

Background Fatigue of unknown origin is a hallmark symptom in chronic fatigue syndrome (CFS) and also found 20% hypothyroidism patients despite appropriate levothyroxine treatment. Here, we suggest that these disorders, peripheral serotonin levels are low, elevating them to normal range with L-carnitine accompanied reduced fatigue. Methods We conducted retrospective analysis follow-up clinical data (CFS N=12; N=40) where serum were compared before vs. after 7 weeks oral supplementation. Results After L-carnitine, increased (8-fold CFS, Sig. = 0.002, 6-fold hypothyroidism, < 0.001) whereas decreased (2-fold both CFS 0.002 for 0.001 hypothyroidism). There was negative correlation between level (for rho -0.49 -0.67 L-carnitine; -0.24 -0.83 L-carnitine). Conclusions These findings new link low serotonin,

Language: Английский

Citations

7
The Active Ingredient Catalpol in Rehmannia glutinosa Reduces Blood Glucose in Diabetic Rats via the AMPK Pathway DOI Creative Commons
Li Yang, Qiang Chen, H.J. Sun

et al.

Diabetes Metabolic Syndrome and Obesity, Journal Year: 2024, Volume and Issue: Volume 17, P. 1761 - 1767

Published: April 1, 2024

Background: Type 2 diabetes mellitus (T2DM) poses a huge threat to population health globally, and more drugs need be explored for treatment. In this study, we investigated the mechanism of active ingredient catalpol in Rehmannia glutinosa on reduces blood glucose diabetic. Methods: The T2DM model was constructed by intraperitoneal injection streptozotocin into Sprague-Dawley (SD) rats, which were randomly grouped group, pioglitazone high-dose low-dose group normal control group.The intervention continued 28 d, changes body weight, fasting glucose, insulin lipid levels observed. Results: Of all drugs, had most pronounced hypoglycemic effect, began decline after weeks treatment no effect group. Among them, able increase serum triglyceride level, effectively reduced total cholesterol level rats. low dose decreased concentration low-density lipoprotein (LDL), while high increased LDL. Conclusion: As an , has potential lower improve lipids treatment, its action may achieved regulating adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, provides new idea development therapeutic approaches. Keywords: catalpol, type diabetes, traditional Chinese medicine

Language: Английский

Citations

5
A nutrigeroscience approach: Dietary macronutrients and cellular senescence DOI
Mariah F. Calubag, Paul D. Robbins, Dudley W. Lamming

et al.

Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(9), P. 1914 - 1944

Published: Aug. 23, 2024

Language: Английский

Citations

5