Astragaloside IV Protects against Diabetic Nephropathy by Inhibiting FUNDC1‐Dependent Mitochondria‐Associated Endoplasmic Reticulum Membranes DOI Creative Commons
Zeng Zhang,

Yanyan Wang,

Fengzhu Zhou

et al.

Journal of Food Biochemistry, Journal Year: 2024, Volume and Issue: 2024(1)

Published: Jan. 1, 2024

Studies have demonstrated the potential therapeutic effects of Astragaloside IV (AS‐IV) in various diseases. However, its effect on diabetic nephropathy (DN) and underlying mechanisms are not clear. The expression FUNDC1 DN patients high glucose‐induced human renal tubular epithelial cell line (HK‐2) with or without AS‐IV was analyzed using quantitative real‐time polymerase chain reaction Western blot. Cell Counting Kit‐8 (CCK‐8) assay used to quantify viability. intracellular oxygen consumption rate measured by seahorse energy analyzer, mitochondrial reactive species Ca 2+ levels were determined flow cytometry. A mice model diabetes constructed treated different doses AS‐IV. Hematoxylin‐eosin Masson staining examine pathological changes tissue. Creatinine, blood urea nitrogen, urinary protein detected biochemical method. results increased glucose‐cultured HK‐2 cells. silencing inhibited mitochondria‐associated endoplasmic reticulum (ER) membrane formation dysfunction Importantly, treatment FUNDC1‐induced ER also protected against injury improved function mice. alleviates progression inhibiting FUNDC1‐dependent membrane.

Language: Английский

The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease DOI Creative Commons
Sarah X. Zhang, Josh J. Wang, Christopher R. Starr

et al.

Progress in Retinal and Eye Research, Journal Year: 2023, Volume and Issue: 98, P. 101231 - 101231

Published: Dec. 12, 2023

Language: Английский

Citations

24
Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment DOI Creative Commons
Yong Liu,

Jin-Ling Huo,

Kaidi Ren

et al.

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: March 20, 2024

Abstract Diabetic cardiomyopathy (DCM), an important complication of diabetes mellitus (DM), is one the most serious chronic heart diseases and has become a major cause failure worldwide. At present, pathogenesis DCM unclear, there still lack effective therapeutics. Previous studies have shown that homeostasis mitochondria endoplasmic reticulum (ER) play core role in maintaining cardiovascular function, structural functional abnormalities these organelles seriously impact occurrence development various diseases, including DCM. The interplay between ER mediated by mitochondria-associated membrane (MAM), which participates regulating energy metabolism, calcium homeostasis, mitochondrial dynamics, autophagy, stress, inflammation, other cellular processes. Recent proven MAM closely related to initiation progression In this study, we aim summarize recent research progress on MAM, elaborate key DCM, discuss potential as therapeutic target for thereby providing theoretical reference basic clinical treatment.

Language: Английский

Citations

12
Novel insight into the role of A-kinase anchoring proteins (AKAPs) in ischemic stroke and therapeutic potentials DOI Open Access

Ziyu He,

Letian Xie,

Jiyong Liu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 175, P. 116715 - 116715

Published: May 12, 2024

Ischemic stroke, a devastating disease associated with high mortality and disability worldwide, has emerged as an urgent public health issue. A-kinase anchoring proteins (AKAPs) are group of signal-organizing molecules that compartmentalize anchor wide range receptors effector have major role in stabilizing mitochondrial function promoting neurodevelopmental development the central nervous system (CNS). Growing evidence suggests dysregulation AKAPs expression activity is closely oxidative stress, ion disorder, dysfunction, blood-brain barrier (BBB) impairment ischemic stroke. However, underlying mechanisms remain inadequately understood. This review provides comprehensive overview composition structure protein (AKAP) family members, emphasizing their physiological functions CNS. We explored depth molecular cellular AKAP complexes pathological progression risk factors including hypertension, hyperglycemia, lipid metabolism disorders, atrial fibrillation. Herein, we highlight potential pharmacological target against stroke hope inspiring translational research innovative clinical approaches.

Language: Английский

Citations

6
Broadening horizons: the contribution of mitochondria-associated endoplasmic reticulum membrane (MAM) dysfunction in diabetic kidney disease DOI Creative Commons
Yong Liu,

Yingjin Qiao,

Shaokang Pan

et al.

International Journal of Biological Sciences, Journal Year: 2023, Volume and Issue: 19(14), P. 4427 - 4441

Published: Jan. 1, 2023

Diabetic kidney disease (DKD) is a global health issue that presents complex pathogenesis and limited treatment options.To provide guidance for precise therapies, it crucial to accurately identify the of DKD.Several studies have recognized mitochondrial endoplasmic reticulum (ER) dysfunction are key drivers DKD.The mitochondria-associated ER membrane (MAM) dynamic contact site (MSC) connects mitochondria essential in maintaining normal function two organelles.MAM involved various cellular processes, including lipid synthesis transport, calcium homeostasis, fusion fission, stress.Meanwhile, recent confirm MAM plays significant role DKD by regulating glucose metabolism, inflammation, stress, fission fusion, autophagy.Herein, this review aims comprehensive summary physiological MAMs their impact on progression DKD.Subsequently, we discuss trend pharmaceutical target resident proteins treating DKD.Furthermore, also explore future development prospects research, thereby providing new perspective basic clinical DKD.

Language: Английский

Citations

14
The role of endoplasmic reticulum–mitochondria-associated membranes in diabetic kidney disease DOI Open Access
Ahmed Elwakiel, Akash Mathew, Berend Isermann

et al.

Cardiovascular Research, Journal Year: 2023, Volume and Issue: 119(18), P. 2875 - 2883

Published: Dec. 1, 2023

Abstract Diabetic kidney disease (DKD) is the leading cause of end-stage renal worldwide. The pathomechanisms DKD are multifactorial, yet haemodynamic and metabolic changes in early stages appear to predispose towards irreversible functional loss histopathological changes. Recent studies highlight importance endoplasmic reticulum–mitochondria-associated membranes (ER-MAMs), structures conveying important cellular homeostatic effects, pathology DKD. Disruption ER-MAM integrity diabetic kidneys associated with progression, but regulation ER-MAMs their pathogenic contribution remain largely unknown. Exploring cell-specific components dynamic may lead identification new approaches detect stratify patients In addition, these insights novel therapeutic target and/or reverse progression. this review, we discuss association key driving such as insulin resistance, dyslipidaemia, ER stress, inflammasome activation further exploration diagnostic targets

Language: Английский

Citations

10
CDK4 inactivation inhibits apoptosis via mitochondria-ER contact remodeling in triple-negative breast cancer DOI Creative Commons
Dorian V. Ziegler, Kanishka Parashar, Lucía C. Leal-Esteban

et al.

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

Published: Jan. 9, 2025

Language: Английский

Citations

0
Inhibition of SGLT2 protects podocytes in diabetic kidney disease by rebalancing mitochondria-associated endoplasmic reticulum membranes DOI Creative Commons
Xue Li, Qiong Li,

Xinying Jiang

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Nov. 7, 2024

Sodium-glucose cotransporter 2 (SGLT2) inhibitors have changed the therapeutic landscape for diabetic kidney disease (DKD) patients, but their underlying mechanisms are complicated and not fully understood. Mitochondria-associated endoplasmic reticulum membranes (MAMs), dynamic contact sites between mitochondria (ER), serve as intracellular platforms important regulating cellular fate function. This study explored roles of SGLT2 in MAMs formation podocytes.

Language: Английский

Citations

3
Mitochondrial dysfunction in diabetic nephropathy: insights and therapeutic avenues from traditional Chinese medicine DOI Creative Commons

Dan-mai Zhao,

Rui Zhong, Xiaotian Wang

et al.

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

Published: July 23, 2024

Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus. The progressive damage to glomeruli, tubules, and interstitium in the kidneys can lead development chronic kidney disease (CKD) end-stage renal (ESRD). Most energy we need comes from mitochondria. Mitochondria are best known as sites for production respiratory ATP essential eukaryotic life. pathogenesis DN involves variety factors, such altered haemodynamics, oxidative stress, inflammation, studies animal models suggest that mitochondrial dysfunction plays an important role DN. Traditional Chinese medicine (TCM) has history more than 2,500 years rich experience remarkable efficacy treatment Recent have found TCM may great potential regulating This review will elucidate main causes relationship with DN, explore depth mechanisms protect by improving dysfunction. Current pharmacological treatments patients do not prevent inevitable progression ESRD. With herbs, expected be most promising candidate continue learn about incorporate current advances extraction techniques.

Language: Английский

Citations

2
ER Stress-Perturbed Intracellular Protein O-GlcNAcylation Aggravates Podocyte Injury in Diabetes Nephropathy DOI Open Access

Shicong Song,

Tiantian Hu,

Xu Shi

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(24), P. 17603 - 17603

Published: Dec. 18, 2023

Diabetes nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide, and podocyte injury central contributor to progression DN. Despite emerging evidence that has established importance endoplasmic reticulum (ER) stress in pathogenesis DN, abnormal protein O-GlcNAcylation also augmented. Currently, mechanism associating these two hyperglycemia-induced disorders remains poorly understood. This study intended elucidate whether ER drives hyper-protein We used both type 1 2 DN models confirm occurrence excessive O-GlcNAcylation, then purification was conducted for further investigation. Nephroseq V5 data were mined vitro studies applied reveal involvement hyper-O-GlcNAcylation injury. Our results indicated induced human RNA-seq from showed O-GlcNAcylation-related genes significantly upregulated patients. demonstrated occurred prior hyper-O-GlcNAc modification pharmacologically inhibited can help decrease apoptosis by hyperglycemia. Together, discoveries will aid uncovering activation stress-O-GlcNAcylation axis under which open up new therapeutic approaches preventing progression.

Language: Английский

Citations

4
Biofactors regulating mitochondrial function and dynamics in podocytes and podocytopathies DOI
Seyyedeh Mina Hejazian, Mohammadreza Ardalan, Seyed Mahdi Hosseiniyan Khatibi

et al.

Journal of Cellular Physiology, Journal Year: 2023, Volume and Issue: 238(10), P. 2206 - 2227

Published: Sept. 2, 2023

Podocytes are terminally differentiated kidney cells acting as the main gatekeepers of glomerular filtration barrier; hence, inhibiting proteinuria. Podocytopathies classified diseases caused by podocyte damage. Different genetic and environmental risk factors can cause damage death. Recent evidence shows that mitochondrial dysfunction also contributes to Understanding alterations in metabolism function podocytopathies whether altered homeostasis/dynamics is a or effect issues need in-depth studies. This review highlights roles mitochondria their bioenergetics podocytes. Then, factors/signalings regulate podocytes discussed. After that, role reviewed injury development different podocytopathies. Finally, therapeutic targets considered.

Language: Английский

Citations

2