Mitochondrial homeostasis and redox status in cardiovascular diseases : Protective role of the vagal system
Copyright © 2021 Elsevier Inc. All rights reserved..
Mitochondria participate in essential cellular functions, including energy production, metabolism, redox homeostasis regulation, intracellular Ca2+ handling, apoptosis, and cell fate determination. Disruption of mitochondrial homeostasis under pathological conditions results in mitochondrial reactive oxygen species (ROS) generation and energy insufficiency, which further disturb mitochondrial and cellular homeostasis in a deleterious loop. Mitochondrial redox status has therefore become a potential target for therapy against cardiovascular diseases. In this review, we highlight recent progress in determining the roles of mitochondrial processes in regulating mitochondrial redox status, including mitochondrial dynamics (fusion-fission pathways), mitochondrial cristae remodeling, mitophagy, biogenesis, and mitochondrion-organelle interactions (endoplasmic reticulum-mitochondrion interactions, nucleus-mitochondrion communication, and lipid droplet-mitochondrion interactions). The strategies that activate vagal system include direct vagal activation (electrical vagal stimulation and administration of vagal neurotransmitter acetylcholine) and pharmacological modulation (choline and cholinesterase inhibitors). The vagal system plays an important role in maintaining mitochondrial homeostasis and suppressing mitochondrial oxidative stress by promoting mitochondrial biogenesis and mitophagy, moderating mitochondrial fusion and fission, strengthening mitochondrial cristae stabilization, regulating mitochondrion-organelle interactions, and inhibiting mitochondrial Ca2+ overload. Therefore, enhancement of vagal activity can maintain mitochondrial homeostasis and represents a promising therapeutic strategy for cardiovascular diseases.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2022 |
|---|---|
| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:178 |
|---|---|
| Enthalten in: |
Free radical biology & medicine - 178(2022) vom: 15. Jan., Seite 369-379 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
He, Xi [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Cardiovascular diseases |
|---|
| Anmerkungen: |
Date Completed 05.01.2022 Date Revised 05.01.2022 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.freeradbiomed.2021.12.255 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM334431409 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM334431409 | ||
| 003 | DE-627 | ||
| 005 | 20231225223701.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2022 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.freeradbiomed.2021.12.255 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1114.xml |
| 035 | |a (DE-627)NLM334431409 | ||
| 035 | |a (NLM)34906725 | ||
| 035 | |a (PII)S0891-5849(21)01107-2 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a He, Xi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Mitochondrial homeostasis and redox status in cardiovascular diseases |b Protective role of the vagal system |
| 264 | 1 | |c 2022 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 05.01.2022 | ||
| 500 | |a Date Revised 05.01.2022 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2021 Elsevier Inc. All rights reserved. | ||
| 520 | |a Mitochondria participate in essential cellular functions, including energy production, metabolism, redox homeostasis regulation, intracellular Ca2+ handling, apoptosis, and cell fate determination. Disruption of mitochondrial homeostasis under pathological conditions results in mitochondrial reactive oxygen species (ROS) generation and energy insufficiency, which further disturb mitochondrial and cellular homeostasis in a deleterious loop. Mitochondrial redox status has therefore become a potential target for therapy against cardiovascular diseases. In this review, we highlight recent progress in determining the roles of mitochondrial processes in regulating mitochondrial redox status, including mitochondrial dynamics (fusion-fission pathways), mitochondrial cristae remodeling, mitophagy, biogenesis, and mitochondrion-organelle interactions (endoplasmic reticulum-mitochondrion interactions, nucleus-mitochondrion communication, and lipid droplet-mitochondrion interactions). The strategies that activate vagal system include direct vagal activation (electrical vagal stimulation and administration of vagal neurotransmitter acetylcholine) and pharmacological modulation (choline and cholinesterase inhibitors). The vagal system plays an important role in maintaining mitochondrial homeostasis and suppressing mitochondrial oxidative stress by promoting mitochondrial biogenesis and mitophagy, moderating mitochondrial fusion and fission, strengthening mitochondrial cristae stabilization, regulating mitochondrion-organelle interactions, and inhibiting mitochondrial Ca2+ overload. Therefore, enhancement of vagal activity can maintain mitochondrial homeostasis and represents a promising therapeutic strategy for cardiovascular diseases | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Cardiovascular diseases | |
| 650 | 4 | |a Mitochondrial homeostasis | |
| 650 | 4 | |a Mitochondrial redox status | |
| 650 | 4 | |a Mitochondrion–organelle interactions | |
| 650 | 4 | |a Vagal activity | |
| 700 | 1 | |a Liu, Jiankang |e verfasserin |4 aut | |
| 700 | 1 | |a Zang, Wei-Jin |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Free radical biology & medicine |d 1989 |g 178(2022) vom: 15. Jan., Seite 369-379 |w (DE-627)NLM012613827 |x 1873-4596 |7 nnns |
| 773 | 1 | 8 | |g volume:178 |g year:2022 |g day:15 |g month:01 |g pages:369-379 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.freeradbiomed.2021.12.255 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 178 |j 2022 |b 15 |c 01 |h 369-379 | ||