scholarly journals Regulation of Mitochondrial Quality Control by Natural Drugs in the Treatment of Cardiovascular Diseases: Potential and Advantages

2020 ◽  
Vol 8 ◽  
Author(s):  
Xing Chang ◽  
Wenjin Zhang ◽  
Zhenyu Zhao ◽  
Chunxia Ma ◽  
Tian Zhang ◽  
...  
Keyword(s):  
Quality Control ◽  
Cardiovascular Diseases ◽  
Respiratory Chain ◽  
Mitochondrial Respiratory Chain ◽  
Therapeutic Effects ◽  
Active Ingredients ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Energy Metabolism ◽  
Natural Drugs ◽  
Mitochondrial Respiratory

Mitochondria are double-membraned cellular organelles that provide the required energy and metabolic intermediates to cardiomyocytes. Mitochondrial respiratory chain defects, structure abnormalities, and DNA mutations can affect the normal function of cardiomyocytes, causing an imbalance in intracellular calcium ion homeostasis, production of reactive oxygen species, and apoptosis. Mitochondrial quality control (MQC) is an important process that maintains mitochondrial homeostasis in cardiomyocytes and involves multi-level regulatory mechanisms, such as mitophagy, mitochondrial fission and fusion, mitochondrial energy metabolism, mitochondrial antioxidant system, and mitochondrial respiratory chain. Furthermore, MQC plays a role in the pathological mechanisms of various cardiovascular diseases (CVDs). In recent years, the regulatory effects of natural plants, drugs, and active ingredients on MQC in the context of CVDs have received significant attention. Effective active ingredients in natural drugs can influence the production of energy-supplying substances in the mitochondria, interfere with the expression of genes associated with mitochondrial energy requirements, and regulate various mechanisms of MQC modulation. Thus, these ingredients have therapeutic effects against CVDs. This review provides useful information about novel treatment options for CVDs and development of novel drugs targeting MQC.

scholarly journals Barth syndrome cellular models have dysregulated respiratory chain complex I and mitochondrial quality control due to abnormal cardiolipin

2021 ◽  
Author(s):  
Arianna Franca Anzmann ◽  
Olivia Sniezek ◽  
Alexandra Pado ◽  
Veronica F. Busa ◽  
Frederic M Vaz ◽  
...  
Keyword(s):  
Quality Control ◽  
Respiratory Chain ◽  
Complex I ◽  
Chain Complex ◽  
Mitochondrial Respiratory Chain ◽  
Barth Syndrome ◽  
Hek293 Cells ◽  
Respiratory Chain Complex ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Quality Control

Barth syndrome (BTHS) is an X-linked genetic condition caused by defects in TAZ, which encodes a transacylase involved in the remodeling of the inner mitochondrial membrane phospholipid, cardiolipin (CL). As such, CL has been implicated in numerous mitochondrial functions, and the role of defective CL in the clinical pathology of BTHS is under intense investigation. We used untargeted proteomics, shotgun lipidomics, gene expression analysis, and targeted metabolomics to identify novel areas of mitochondrial dysfunction in a new model of TAZ deficiency in HEK293 cells. Functional annotation analysis of proteomics data revealed abnormal regulation of mitochondrial respiratory chain complex I (CI), driven by the reduced abundance of 6 CI associated proteins in TAZ-deficient HEK293 cells: MT-ND3, NDUFA5, NDUFAB1, NDUFB2, NDUFB4, and NDUFAF1. This resulted in reduced assembly and function of CI in TAZ-deficient HEK293 cells as well as BTHS patient derived lymphoblast cells. We also identified increased abundance of PARL, a rhomboid protein involved in the regulation of mitophagy and apoptosis, and abnormal downstream processing of PGAM5, another mediator of mitochondrial quality control, in TAZ-deficient cells. Lastly, we modulated CL via the phospholipase inhibitor bromoenol lactone and the CL targeted SS-peptide, SS-31, and showed that each is able to remediate abnormalities in CI abundance as well as PGAM5 processing. Thus, mitochondrial respiratory chain CI and PARL/PGAM5 regulated mitochondrial quality control, both of whose functions localize to the inner mitochondrial membrane, are dysregulated due to TAZ deficiency and are partially remediated via modulation of CL.

Nanosized non-proteinaceous complexes III and IV mimicking electron transfer of mitochondrial respiratory chain

2021 ◽  
Author(s):  
Iago A. Modenez ◽  
Lucyano J.A. Macedo ◽  
Antonio F.A.A. Melo ◽  
Andressa R. Pereira ◽  
Osvaldo N. Oliveira Jr ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Respiratory Chain ◽  
Mitochondrial Respiratory Chain ◽  
Mitochondrial Respiratory

scholarly journals Na+ controls hypoxic signalling by the mitochondrial respiratory chain

2021 ◽  
Vol 165 ◽  
pp. 18
Author(s):  
Pablo Hernansanz-Agustín ◽  
Carmen Choya-Foces ◽  
José Antonio Enríquez ◽  
Antonio Martínez-Ruiz
Keyword(s):  
Respiratory Chain ◽  
Mitochondrial Respiratory Chain ◽  
Mitochondrial Respiratory
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