Pharmacology of mitochondrial permeability transition pore inhibitors

Naryzhnaya, N. V.; Маслов, Л Н; Oeltgen, Peter R.

doi:10.1002/ddr.21593

Cited by 26 publications

(22 citation statements)

References 180 publications

(268 reference statements)

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“…The opening of mPTP is a vital event that causes cell death . To elucidate the underlying mechanism of complex-induced apoptosis, we explored its possible effects on mitochondrial functions.…”

Section: Resultsmentioning

confidence: 99%

Rhodium(III)–Picolinamide Complexes Act as Anticancer and Antimetastasis Agents via Inducing Apoptosis and Autophagy

Yang

et al. 2023

J. Med. Chem.

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As a continuation of our endeavors in discovering metal-based drugs with cytotoxic and antimetastatic activities, herein, we reported the syntheses of 11 new rhodium(III)–picolinamide complexes and the exploration of their potential anticancer activities. These Rh(III) complexes showed high antiproliferative activity against the tested cancer cell lines in vitro. The mechanism study indicated that Rh1 ([Rh(3a)(CH3CN)Cl2]) and Rh2 ([Rh(3b)(CH3CN)Cl2]) inhibited cell proliferation by multiple modes of action via cell cycle arrest, apoptosis, and autophagy and inhibited cell metastasis via FAK-regulated integrin β1-mediated suppression of EGFR expression. Furthermore, Rh1 and Rh2 significantly inhibited bladder cancer growth and breast cancer metastasis in a xenograft model. These rhodium(III) complexes could be developed as potential anticancer agents with antitumor growth and antimetastasis activity.

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Section: Resultsmentioning

confidence: 99%

Rhodium(III)–Picolinamide Complexes Act as Anticancer and Antimetastasis Agents via Inducing Apoptosis and Autophagy

Yang

et al. 2023

J. Med. Chem.

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“…By contrast, MMP and mitochondrial ca 2+ concentrations are the principal drivers of mPTP opening, resulting in the release of cytochrome c and other substances associated with cell death into the cytosol (191,192,(194)(195)(196)(197). This leads to mitochondrial swelling and reduced mitochondrial respiratory chain activity, which can cause various diseases, such as neurodegenerative diseases and cancers (190,(198)(199)(200). Furthermore, studies have shown that PINK1 can inhibit mPTP opening by downregulating intracellular ROS levels, suggesting that mitochondrial autophagy serves a regulatory role in mPTP opening (191)(192)(193).…”

Section: Detection Of Mitochondrial Permeability Transition Poresmentioning

confidence: 99%

Common methods in mitochondrial research (Review)

Yin

Shen

2022

Int J Mol Med

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Mitochondrial abnormalities are primarily seen in morphology, structure and function. They can cause damage to organs, including the heart, brain and muscle, by various mechanisms, such as oxidative stress, abnormal energy metabolism, or genetic mutations. Identifying and detecting pathophysiological alterations in mitochondria is the principal means of studying mitochondrial abnormalities. The present study reviewed methods in mitochondrial research and focused on three aspects: Mitochondrial extraction and purification, morphology and structure and function. In addition to classical methods, such as electron microscopy and mitochondrial membrane potential monitoring, newly developed methods, such as mitochondrial ultrastructural determination, mtdNA mutation assays, metabolomics and analyses of regulatory mechanisms, have also been utilized in recent years. These approaches enable the accurate detection of mitochondrial abnormalities and provide guidance for the diagnosis and treatment of related diseases. Contents1. Introduction 2. Extraction and purification of mitochondria 3. determination of mitochondrial morphology and structure 4. determination of mitochondrial function 5.

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“…105 MPT pore opining induces apoptosis of cardiomyocytes, MPT pore closing prevents ischemic/reperfusion injury of the heart. 162 It has been shown that the cardioprotective effect of BNP at cardiac reperfusion is mediated via MPT pore closing. 73 There are data that ANP prevents MPT pore opening in H9c2 cardiomyoblasts.…”

Section: Natriuretic Peptides K Atp Channels and Mpt Porementioning

confidence: 99%

The Role of Natriuretic Peptides in the Regulation of Cardiac Tolerance to Ischemia/Reperfusion and Postinfarction Heart Remodeling

Tsibulnikov

Mukhomedzyanov

Boshchenko

et al. 2020

J Cardiovasc Pharmacol Ther

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In the past 10 years, mortality from acute myocardial infarction has not decreased despite the widespread introduction of percutaneous coronary intervention. The reason for this situation is the absence in clinical practice of drugs capable of preventing reperfusion injury of the heart with high efficiency. In this regard, noteworthy natriuretic peptides (NPs) which have the infarct-limiting effect, prevent reperfusion cardiac injury, prevent adverse post-infarction remodeling of the heart. Atrial natriuretic peptide does not have the infarct-reducing effect in rats with alloxan-induced diabetes mellitus. NPs have the anti-apoptotic and anti-inflammatory effects. There is indirect evidence that NPs inhibit pyroptosis and autophagy. Published data indicate that NPs inhibit reactive oxygen species production in cardiomyocytes, aorta, heart, kidney and the endothelial cells. NPs can suppress aldosterone, angiotensin II, endothelin-1 synthesize and secretion. NPs inhibit the effects aldosterone, angiotensin II on the post-receptor level through intracellular signaling events. NPs activate guanylyl cyclase, protein kinase G and protein kinase A, and reduce phosphodiesterase 3 activity. NO-synthase and soluble guanylyl cyclase are involved in the cardioprotective effect of NPs. The cardioprotective effect of natriuretic peptides is mediated via activation of kinases (AMPK, PKC, PI3 K, ERK1/2, p70s6 k, Akt) and inhibition of glycogen synthase kinase 3β. The cardioprotective effect of NPs is mediated via sarcolemmal KATP channel and mitochondrial KATP channel opening. The cardioprotective effect of brain natriuretic peptide is mediated via MPT pore closing. The anti-fibrotic effect of NPs may be mediated through inhibition TGF-β1 expression. Natriuretic peptides can inhibit NF-κB activity and activate GATA. Hemeoxygenase-1 and peroxisome proliferator-activated receptor γ may be involved in the infarct-reducing effect of NPs. NPs exhibit the infarct-limiting effect in patients with acute myocardial infarction. NPs prevent post-infarction remodeling of the heart. To finally resolve the question of the feasibility of using NPs in AMI, a multicenter, randomized, blind, placebo-controlled study is needed to assess the effect of NPs on the mortality of patients after AMI.

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Pharmacology of mitochondrial permeability transition pore inhibitors

Cited by 26 publications

References 180 publications

Rhodium(III)–Picolinamide Complexes Act as Anticancer and Antimetastasis Agents via Inducing Apoptosis and Autophagy

Rhodium(III)–Picolinamide Complexes Act as Anticancer and Antimetastasis Agents via Inducing Apoptosis and Autophagy

Common methods in mitochondrial research (Review)

The Role of Natriuretic Peptides in the Regulation of Cardiac Tolerance to Ischemia/Reperfusion and Postinfarction Heart Remodeling

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