piRNAs and miRNAs Can Bind to mRNA of <i>KLOTHO</i> and <i>FGF23</i> Genes DOI Open Access
Ivashchenko At,

Kyrmyzy Akhmetova,

Murat Zhanuzakov

et al.

Published: June 14, 2023

The problem of increasing life expectancy is solved with the help many medical and social areas. It has been established that piRNAs miRNAs can significantly modify expression protein-coding genes by suppressing translation process. aim this work was to establish possibility binding mRNA KLOTHO FGF23 genes, which promote health increase through participation in key metabolic processes. We used MirTarget program, determines quantitative characteristics complementary interactions all nucleotides genes. piR-44682, piR-1940042, piR-3008660, piR-3215034, piR-6885965, piR-7980636 one miRNA (ID00756.3p-miR) gene were found cluster sites (BSs). piRNA-6890096 interacted a fully manner using only canonical nucleotides. Among 17494 human target interacting five bind identified. AFF2, BCL2L11, CPT1A, DAZAP1, NDRG3, SKIDA1, WBP4, ZIC5, ZSWIM6 piR-3215034 formed clusters BSs located 5'UTR, CDS 3'UTR. piR-576442, piR-1501557, piR-1845735, piR-2069834, piR-3029987 had mRNAs gene, proposed use as regulators anti-aging

Language: Английский

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells DOI Creative Commons
Azra Kulovic‐Sissawo, Carolina Tocantins, Mariana S. Diniz

et al.

Biology, Journal Year: 2024, Volume and Issue: 13(2), P. 70 - 70

Published: Jan. 23, 2024

Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative it contributes significantly to the global health burden. Recent research indicates a link between risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, endothelial dysfunction. Circulating progenitor cells (EPCs) are recruited into vessel wall maintain appropriate function, repair, angiogenesis. After attachment, EPCs differentiate mature (ECs). Like ECs, also susceptible CVRFs, metabolic chronic inflammation. Therefore, may have long-term effects on function ECs which differentiate, particularly in presence damage. However, CVRFs impaired has hardly been investigated. In this review, we aim consolidate existing knowledge development vascular endothelium, place context recent studies investigating consequences EPCs, discuss role Thus, gain comprehensive understanding mechanisms involved EPC deterioration relation address potential therapeutic interventions targeting promote function.

Language: Английский

Citations

9
The role of mitophagy in metabolic diseases and its exercise intervention DOI Creative Commons

Shaokai Tang,

Yuanwen Geng,

Qinqin Lin

et al.

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

Published: Jan. 29, 2024

Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, maintain cellular homeostasis by removing damaged mitochondria participating developing diseases. Research has confirmed exercise regulate mitophagy levels, thereby exerting protective effects This article reviews role of diseases, on mitophagy, potential mechanisms exercise-regulated intervention providing new insights for future basic clinical research interventions to prevent treat

Language: Английский

Citations

8
Natural Activators of Autophagy DOI

Julia A. Pavlova,

Ekaterina A. Guseva,

О. А. Донцова

et al.

Biochemistry (Moscow), Journal Year: 2024, Volume and Issue: 89(1), P. 1 - 26

Published: Jan. 1, 2024

Language: Английский

Citations

7
MAP4K4 exacerbates cardiac microvascular injury in diabetes by facilitating S-nitrosylation modification of Drp1 DOI Creative Commons
Yuqiong Chen, Su Li, Bo Guan

et al.

Cardiovascular Diabetology, Journal Year: 2024, Volume and Issue: 23(1)

Published: May 9, 2024

Abstract Dynamin-related protein 1 (Drp1) is a crucial regulator of mitochondrial dynamics, the overactivation which can lead to cardiovascular disease. Multiple distinct posttranscriptional modifications Drp1 have been reported, among S-nitrosylation was recently introduced. However, detailed regulatory mechanism (SNO-Drp1) in cardiac microvascular dysfunction diabetes remains elusive. The present study revealed that mitogen-activated kinase 4 (MAP4K4) consistently upregulated diabetic cardiomyopathy (DCM) and promoted SNO-Drp1 endothelial cells (CMECs), turn led disorder. Further studies confirmed MAP4K4 at human C644 (mouse C650) by inhibiting glutathione peroxidase (GPX4) expression, through stimulated ferroptosis diabetes. In contrast, inhibition via DMX-5804 significantly reduced ferroptosis, alleviated improved db/db mice reducing SNO-Drp1. parallel, C650A mutation abolished role promoting disorder dysfunction. conclusion, our findings demonstrate plays an important DCM reveal activation may act as downstream targets, representing potential therapeutic targets for DCM.

Language: Английский

Citations

7
Pinacidil ameliorates cardiac microvascular ischemia–reperfusion injury by inhibiting chaperone-mediated autophagy of calreticulin DOI Creative Commons
Muyin Liu, Su Li, Ming Yin

et al.

Basic Research in Cardiology, Journal Year: 2024, Volume and Issue: 119(1), P. 113 - 131

Published: Jan. 2, 2024

Abstract Calcium overload is the key trigger in cardiac microvascular ischemia–reperfusion (I/R) injury, and calreticulin (CRT) a calcium buffering protein located endoplasmic reticulum (ER). Additionally, role of pinacidil, an antihypertensive drug, protecting microcirculation against I/R injury has not been investigated. Hence, this study aimed to explore benefits pinacidil on with focus endothelial homeostasis CRT signaling. Cardiac vascular perfusion no-reflow area were assessed using FITC–lectin assay Thioflavin-S staining. Endothelial homeostasis, CRT–IP3Rs–MCU signaling expression, apoptosis by real-time signal reporter GCaMP8, western blotting, fluorescence Drug affinity-responsive target stability (DARTS) was adopted detect proteins that directly bind pinacidil. The present found treatment improved capillary density perfusion, reduced infraction areas, function hemodynamics after injury. These attributed ability alleviate mitochondria-dependent cells (CMECs). Moreover, DARTS showed binds HSP90, through which it inhibits chaperone-mediated autophagy (CMA) degradation CRT. overexpression inhibited IP3Rs MCU mitochondrial inflow suppressed apoptosis. Importantly, endothelial-specific shared similar cardiovascular protection In conclusion, our data indicate attenuated potentially improving overload.

Language: Английский

Citations

6
Dual-specificity phosphatase 1 interacts with prohibitin 2 to improve mitochondrial quality control against type-3 cardiorenal syndrome DOI Creative Commons
Nanyang Liu,

Yanqiu Ding,

Hao Zhou

et al.

International Journal of Medical Sciences, Journal Year: 2024, Volume and Issue: 21(3), P. 547 - 561

Published: Jan. 1, 2024

Type-3 cardiorenal syndrome (CRS-3) is acute kidney injury followed by cardiac injury/dysfunction. Mitochondrial may impair myocardial function during CRS-3. Since dual-specificity phosphatase 1 (DUSP1) and prohibitin 2 (PHB2) both promote mitochondrial quality control, we assessed whether these proteins were dysregulated CRS-3-related depression. We found that DUSP1 was downregulated in heart tissues from a mouse model of transgenic (DUSP1

Language: Английский

Citations

4
THBru attenuates diabetic cardiomyopathy by inhibiting RAGE-dependent inflammation DOI

Henghui Xu,

Sheng-xin Hao,

Heyang Sun

et al.

Acta Pharmacologica Sinica, Journal Year: 2024, Volume and Issue: 45(10), P. 2107 - 2118

Published: June 11, 2024

Language: Английский

Citations

4
MiR-21-3p inhibitor exerts myocardial protective effects by altering macrophage polarization state and reducing excessive mitophagy DOI Creative Commons
Yujing Huang,

Ya-Lin Huang,

Zhaoling Cai

et al.

Communications Biology, Journal Year: 2024, Volume and Issue: 7(1)

Published: Oct. 22, 2024

Chronic heart failure (CHF) is closely associated with inflammation and mitochondrial dysfunction in cardiomyocytes. This study attempts to investigate the effects of microRNA-21-3p (miR-21-3p) on macrophage polarization mitophagy CHF. Here we found miR-21-3p was upregulated CHF negatively correlated carnitine palmitoyl transferase 1A (CPT1A). L-palmitoyl (L-PC) exacerbated isoproterenol (ISO)-induced myocardial structural disruption fibrosis rats, which by miR-21-3p. Mechanistically, accelerated M1 polarization. Both inhibitor CPT1A overexpression suppressed mitophagy. The inhibition reversed MiR-21-3p targeted mRNA co-localized protein In co-culture system macrophages H9c2 cells, mimics cells promoted polarization, whereas reduced phenotype. cell damage. These findings support potential therapeutic targeting regulate inducing Binding fatty acid metabolism-related target gene affects development chronic failure.

Language: Английский

Citations

4
Empagliflozin in diabetic cardiomyopathy: elucidating mechanisms, therapeutic potentials, and future directions DOI

Aiswarya Jaiswal,

Poonam Yadav, Pushkar Singh Rawat

et al.

Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)

Published: Jan. 24, 2025

Language: Английский

Citations

0
Important regulatory role of mitophagy in diabetic microvascular complications DOI Creative Commons
Xiaohan Hu, Jiao Lv, Yunyun Zhao

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 4, 2025

Microvascular complications of diabetes pose a significant threat to global health, mainly including diabetic kidney disease (DKD), retinopathy (DR), peripheral neuropathy (DPN), and cardiomyopathy (DCM), which can ultimately lead failure, blindness, disability, heart failure. With the increasing prevalence diabetes, search for new therapeutic targets microvascular is imminent. Mitophagy widespread strictly maintained process self-renewal energy metabolism that plays an important role in reducing inflammatory responses, inhibiting reactive oxygen species accumulation, maintaining cellular metabolism. Hyperglycemia results impaired mitophagy, leads mitochondrial dysfunction exacerbates progression. This article summarizes relevant molecular mechanisms mitophagy reviews current status research on regulating as potential treatment complications, attempting give angles complications.

Language: Английский

Citations

0