FUNDC1 mediated mitochondria-dependent ferroptosis of epithelial cells in model of asthma by FBXL2/ar/GPX4 signaling pathway of SUMO1 at K136 DOI
Li Li, Xingxing Zhu, Jiayi Zhao

et al.

International Reviews of Immunology, Journal Year: 2024, Volume and Issue: 44(2), P. 45 - 57

Published: Sept. 25, 2024

This study aimed to explore the critical role of FUNDC1 on epithelial cells in model asthma. Patients with asthma and normal healthy volunteers were obtained from our hospital. The serum mRNA expression was down-regulated patients Meanwhile, positive correlation IgE anti-HDM protein. lung tissue mice decreased Sh-FUNDC1 enhanced up-regulation reduced IL-4, IL-5, IL-10 IL-13 activity levels vitro asthma.FUNDC1 down-regulation promoted ferroptosis through inhibition mitochondrial damage. induced FBXL2 AR protein interlinked is modified by SUMO1 at K136. FBXL2, ASN-205, GLN-204, ARG-235, GLN-237 form hydrogen bonds FUNDC1's ASP-15, ASP-16, GLU-25, ARG-29, lengths 2.3, 3.1, 2.9, 2.9 Å, respectively. induction effects Overall, prevents airway FBXL2/AR/GPX4 signaling pathway might benefit treatment or other pulmonary disease.

Language: Английский

Zishenhuoxue decoction-induced myocardial protection against ischemic injury through TMBIM6-VDAC1-mediated regulation of calcium homeostasis and mitochondrial quality surveillance DOI
Xing Chang, Siyuan Zhou, Jinfeng Liu

et al.

Phytomedicine, Journal Year: 2023, Volume and Issue: 132, P. 155331 - 155331

Published: Dec. 31, 2023

Language: Английский

Citations

40
Hormonal orchestra: mastering mitochondria's role in health and disease DOI
Ebtesam A. Al-Suhaimi, Rahaf Alquwaie,

Reem AlSaqabi

et al.

Endocrine, Journal Year: 2024, Volume and Issue: 86(3), P. 903 - 929

Published: Aug. 22, 2024

Language: Английский

Citations

6
Therapeutic Effects of Mesenchymal Stromal Cells Require Mitochondrial Transfer and Quality Control DOI Open Access

Avinash Naraiah Mukkala,

Mirjana Jerkic,

Zahra Khan

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(21), P. 15788 - 15788

Published: Oct. 31, 2023

Due to their beneficial effects in an array of diseases, Mesenchymal Stromal Cells (MSCs) have been the focus intense preclinical research and clinical implementation for decades. MSCs multilineage differentiation capacity, support hematopoiesis, secrete pro-regenerative factors exert immunoregulatory functions promoting homeostasis resolution injury/inflammation. The main include modulation immune cells (macrophages, neutrophils, lymphocytes), secretion antimicrobial peptides, transfer mitochondria (Mt) injured cells. These actions can be enhanced by priming (i.e., licensing) prior exposure deleterious microenvironments. Preclinical evidence suggests that therapeutic a variety pathological states, including cardiac, respiratory, hepatic, renal, neurological diseases. One key emerging is improvement mitochondrial tissues enhancing quality control (MQC). Recent advances understanding cellular MQC, biogenesis, mitophagy, fission, fusion, helped uncover how enhance these processes. Specifically, suggested regulate peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC1α)-dependent Parkin-dependent Mitofusins (Mfn1/2) or Dynamin Related Protein-1 (Drp1)-mediated fission/fusion. In addition, previous studies also verified from through tunneling nanotubes via microvesicular transport. Combined, improve functions, thereby contributing injury inflammation. Thus, uncovering affect MQC opens new avenues organ injury, transplantation MSC-derived might represent attractive approach.

Language: Английский

Citations

15
Mitochondrial Kinase Signaling for Cardioprotection DOI Open Access

Kerstin Boengler,

Chantal Eickelmann, Petra Kleinbongard

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4491 - 4491

Published: April 19, 2024

Myocardial ischemia/reperfusion injury is reduced by cardioprotective adaptations such as local or remote ischemic conditioning. The stimuli activate signaling cascades, which converge on mitochondria and maintain the function of organelles, critical for cell survival. cascades include not only extracellular molecules that sarcolemmal receptor-dependent -independent protein kinases signal at plasma membrane in cytosol, but also involve kinases, are located to within mitochondria, phosphorylate mitochondrial target proteins, thereby modify, e.g., respiration, generation reactive oxygen species, calcium handling, dynamics, mitophagy, apoptosis. In present review, we give a personal opinionated overview selected localized to/within myocardial summarize available data their role protection from it. We highlight regulation these kinases.

Language: Английский

Citations

4
Mitochondrial carrier homolog 2 is important for mitochondrial functionality and non-small cell lung cancer cell growth DOI Creative Commons
Yong Zhao, Siyang Wu,

Guohong Cao

et al.

Cell Death and Disease, Journal Year: 2025, Volume and Issue: 16(1)

Published: Feb. 13, 2025

Language: Английский

Citations

0
CPT1A-mediated MFF succinylation promotes stemness maintenance in ovarian cancer stem cells DOI Creative Commons

Yaqin Zhu,

Shuting Chen,

Hong Su

et al.

Communications Biology, Journal Year: 2025, Volume and Issue: 8(1)

Published: Feb. 16, 2025

Cancer stem cells (CSCs) play crucial roles in cancer progression, immune evasion, drug resistance, and recurrence. Understanding the mechanisms behind CSCs generation stemness maintenance is vital for early diagnosis treatment. Here, we unveil that carnitine palmitoyltransferase 1A (CPT1A) highly expressed ovarian (OCSCs) essential maintaining by regulating lipid desaturation. Studies confirmed CPT1A enhances SREBP1 activation, upregulating SCD1 expression, promoting desaturation OCSCs. Mechanistic studies reveal promotes succinylation of mitochondrial fission factor (MFF) through its lysine succinyltransferase (LSTase) activity, mitochondria-associated membranes formation activation. Inhibiting CPT1A's LSTase activity with Glyburide reduces OCSCs' cisplatin's anti-tumor effects against vitro vivo. Together, our highlight significance stemness, offering potential targets therapeutic strategies Carnitine found to promote mediating succinylation.

Language: Английский

Citations

0
Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease DOI Creative Commons
Kaiqing Li, Xue Xia, Ying Tong

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Oct. 9, 2024

This article reviews the latest research progress on role of mitochondrial autophagy receptor FUN14 domain containing 1 (FUNDC1) in events and kidney disease. FUNDC1 is a protein located outer membrane mitochondria, which maintains function quality mitochondria by regulating autophagy, that is, selective degradation process mitochondria. The structural characteristics enable it to respond intracellular signal changes regulate activity through phosphorylation dephosphorylation. During phosphorylation, unc-51-like kinase (ULK1) promotes activation mitophagy phosphorylating Ser17 FUNDC1. In contrast, Src CK2 kinases inhibit interaction between LC3 Tyr18 Ser13, thereby inhibiting mitophagy. dephosphorylation, PGAM5 phosphatase enhances dephosphorylating activating BCL2L1 inhibits interacting with PGAM5, preventing dephosphorylation plays an important events, participating fission, maintaining homeostasis iron proteins matrix, mediating crosstalk endoplasmic reticulum lysosomes, have effects cell energy metabolism programmed death. aspect disease, abnormal closely related occurrence development many diseases. acute injury (AKI), cardiorenal syndrome (CRS), diabetic nephropathy (DN), chronic disease (CKD) ,renal fibrosis (RF) renal anemia, FUNDC1-mediated imbalance may be one key factors progression. Therefore, in-depth study regulatory mechanism great significance for understanding pathogenesis developing new treatment strategies.

Language: Английский

Citations

3
The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases DOI Creative Commons

Quancheng Han,

Yiding Yu,

Xiujuan Liu

et al.

Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2024

Aging is a major risk factor for cardiovascular diseases (CVD), and mitochondrial autophagy impairment considered significant physiological change associated with aging. Endothelial cells play crucial role in maintaining vascular homeostasis function, participating various processes such as regulating tone, coagulation, angiogenesis, inflammatory responses. As aging progresses, endothelial worsens, leading to the development of numerous diseases. Therefore, vital preventing treating age-related However, there currently lack systematic reviews this area. To address gap, we have written review provide new research therapeutic strategies managing

Language: Английский

Citations

2
Regulation of mitochondria-lysosome interactions in skeletal muscle during exercise, disuse, and aging DOI Creative Commons
Neushaw Moradi, Victoria C. Sanfrancesco, Sabrina Champsi

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 1, 2024

Language: Английский

Citations

2
UCF101 Rescues against Diabetes-Evoked Cardiac Remodeling and Contractile Anomalies through AMPK-Mediated Induction of Mitophagy DOI

Zhiqiang Zhuang,

Yuxi Zhu, Jun Tao

et al.

Pharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 14

Published: Oct. 16, 2024

Introduction: Diabetes mellitus is known to provoke devastating anomalies in myocardial structure and function, while effective therapeutic regimen still lacking. The selective protease inhibitor UCF101 (5-[5-(2-nitrophenyl) furfuryl iodine]-1,3-diphenyl-2-thiobarbituric acid) has been shown fend off ischemic heart injury, although its impact on diabetic cardiomyopathy remains elusive. Methods: Our present work was conducted examine the effect of experimental diabetes-evoked cardiac geometric functional abnormalities as well mechanisms involved. Adult mice were made using streptozotocin (STZ, 50 mg/kg, i.p., for 5 days) receiving (7.15 i.p.). Results: STZ evoked hypertrophy, interstitial fibrosis, mitochondrial ultrastructural damage, oxidative stress, dampened autophagy (LC3B, Beclin 1, elevated p62), mitophagy (FUNDC1 Parkin with upregulated TOM20), increased left ventricular end systolic diameter, reduced fractional shortening, ejection fraction, cardiomyocyte shortening capacity, velocities shortening/re-lengthening, rise intracellular Ca2+ conjunction elongated diastole removal, responses overtly reconciled by little effects from itself. Levels cell injury markers Omi/HtrA2, TNFα, stress signaling (JNK, ERK, p38) enhanced along compromised phosphorylation cellular fuel AMP-activated protein kinase (AMPK) (Thr172) survival molecule GSK3β, downregulated SERCA2a phospholamban, reversed (except SERCA2a). AMPK knockout, pharmacological inhibition, liensinine, parkin knockout nullified UCF101-offered cardioprotection diabetes. STZ-induced upregulation degrading enzymes PP2A PP2C. Conclusion: These findings suggest that rescues diabetes-mediated alterations likely through AMPK-mediated regulation mitophagy.

Language: Английский

Citations

1