Ferulic acid attenuates high glucose-induced MAM alterations via PACS2/IP3R2/FUNDC1/VDAC1 pathway activating proapoptotic proteins and ameliorates cardiomyopathy in diabetic rats

Raj, P. Salin; Nair, Anupama; Rani, Madhu; Rajankutty, K; Sreedharan, Ranjith; Raghu, K.

doi:10.1016/j.ijcard.2022.12.003

Cited by 8 publications

(9 citation statements)

References 57 publications

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“…Recent studies have suggested that there is a close association between MAMs and the development of DCM. Specifically, high glucose-induced aberrations of MAMs and mitochondrial dysfunction have been implicated in the pathogenesis of cardiomyopathy ( Salin Raj et al, 2023 ). One study showed that elevated glucose levels were associated with increased levels of FUNDC1, IP3R2, and MAMs, resulting in mitochondrial dysfunction and increased Ca 2+ transfer ( Wu et al, 2019 ).…”

Section: Mitochondria-associated Endoplasmic Reticulum Membranes Cont...mentioning

confidence: 99%

“…Additionally, researchers discovered that the herbal formula Yiqi Huoxue reduced the Sigma-1 receptor (a chaperone protein on MAMs) and increased IP3R2 expression in infarcted rats, which helped prevent cardiomyocyte hypertrophy ( Lou et al, 2021 ). Another study reported that FeA was found to attenuate MAM alterations induced by high glucose and ameliorate cardiomyopathy in diabetic rats ( Salin Raj et al, 2023 ). This was achieved by activating the pro-apoptotic protein PACS2/IP3R2/FUNDC1/VDAC1 pathway.…”

Section: Mitochondria-associated Endoplasmic Reticulum Membranes As P...mentioning

confidence: 99%

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Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Ding,

Liu,

Zhang

et al. 2024

Front. Pharmacol.

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Cardiovascular diseases (CVDs) are currently the leading cause of death worldwide. In 2022, the CVDs contributed to 19.8 million deaths globally, accounting for one-third of all global deaths. With an aging population and changing lifestyles, CVDs pose a major threat to human health. Mitochondria-associated endoplasmic reticulum membranes (MAMs) are communication platforms between cellular organelles and regulate cellular physiological functions, including apoptosis, autophagy, and programmed necrosis. Further research has shown that MAMs play a critical role in the pathogenesis of CVDs, including myocardial ischemia and reperfusion injury, heart failure, pulmonary hypertension, and coronary atherosclerosis. This suggests that MAMs could be an important therapeutic target for managing CVDs. The goal of this study is to summarize the protein complex of MAMs, discuss its role in the pathological mechanisms of CVDs in terms of its functions such as Ca2+ transport, apoptotic signaling, and lipid metabolism, and suggest the possibility of MAMs as a potential therapeutic approach.

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Section: Mitochondria-associated Endoplasmic Reticulum Membranes Cont...mentioning

confidence: 99%

Section: Mitochondria-associated Endoplasmic Reticulum Membranes As P...mentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Ding,

Liu,

Zhang

et al. 2024

Front. Pharmacol.

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“…Interestingly, AKAP1 has also been found to localize to MAM [ 102 ]. Moreover, it has been reported that high glucose conditions cause MAM aberrations and mitochondrial dysfunction by upregulating PACS2, IP3R2, FUNDC1, and VDAC1, thereby leading to cardiomyocyte apoptosis [ 103 ]. These studies indicate that MAM is involved in the apoptotic process of DCM.…”

Section: Apoptosismentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment

Liu,

Huo,

Ren

et al. 2024

Cell Death Discov.

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

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“…The overabundance of MAMs leads to excessive influx of ER Ca 2+ to mitochondria, thereby triggering a pro-apoptotic signal [58]. This event results in a reduced mitochondrial biogenesis, downregulated the number of respiratory chain complexes, dynamic dysfunction and, ultimately, cellular death [16,59]. Salin and his colleagues hypothesized that ferulic acid and metformin are efficacious against MCM by reducing the formation of excessive MAMs and restoring mitochondrial function via a FUNDC1-related pathway [56].…”

Section: Metabolic Cardiomyopathymentioning

confidence: 99%

FUNDC1: An Emerging Mitochondrial and MAMs Protein for Mitochondrial Quality Control in Heart Diseases

Bai,

Zhang,

et al. 2023

IJMS

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Heart diseases (HDs) are the leading cause of mortality worldwide, with mitochondrial dysfunction being a significant factor in their development. The recently discovered mitophagy receptor, FUNDC1, plays a critical role in regulating the homeostasis of the Mitochondrial Quality Control (MQC) system and contributing to HDs. The phosphorylation of specific regions of FUNDC1 and varying levels of its expression have been shown to have diverse effects on cardiac injury. This review presents a comprehensive consolidation and summary of the latest evidence regarding the role of FUNDC1 in the MQC system. The review elucidates the association of FUNDC1 with prevalent HDs, such as metabolic cardiomyopathy (MCM), cardiac remodeling/heart failure, and myocardial ischemia-reperfusion (IR) injury. The results indicate that the expression of FUNDC1 is elevated in MCM but reduced in instances of cardiac remodeling, heart failure, and myocardial IR injury, with divergent impacts on mitochondrial function among distinct HDs. Exercise has been identified as a powerful preventive and therapeutic approach for managing HDs. Additionally, it has been suggested that exercise-induced enhancement of cardiac function may be attributed to the AMPK/FUNDC1 pathway.

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Ferulic acid attenuates high glucose-induced MAM alterations via PACS2/IP3R2/FUNDC1/VDAC1 pathway activating proapoptotic proteins and ameliorates cardiomyopathy in diabetic rats

Cited by 8 publications

References 57 publications

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment

FUNDC1: An Emerging Mitochondrial and MAMs Protein for Mitochondrial Quality Control in Heart Diseases

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