Targeting Mitochondria in Cardiovascular Diseases
(2016) In Current Pharmaceutical Design 22(37). p.5698-5717- Abstract
BACKGROUND: Cardiovascular diseases (CVDs) are one of the main factors responsible for human morbidity and mortality. Since mitochondria play a critical role in the regulation of cardiac tissue homeostasis, this organelle is a critical target for the protective effects of several pharmaceuticals. Although specific mitochondria-targeted antioxidants and some pharmacological agents are described as potential cardioprotective agents, there are still a few effective mitochondrial therapies for the treatment of CVDs. Agents which have potential cardioprotective effects by directly targeting mitochondria in vitro and in vivo are still in pre-clinical or clinical trials, hence their widespread use in the clinic is still far. Also, some of... (More)
BACKGROUND: Cardiovascular diseases (CVDs) are one of the main factors responsible for human morbidity and mortality. Since mitochondria play a critical role in the regulation of cardiac tissue homeostasis, this organelle is a critical target for the protective effects of several pharmaceuticals. Although specific mitochondria-targeted antioxidants and some pharmacological agents are described as potential cardioprotective agents, there are still a few effective mitochondrial therapies for the treatment of CVDs. Agents which have potential cardioprotective effects by directly targeting mitochondria in vitro and in vivo are still in pre-clinical or clinical trials, hence their widespread use in the clinic is still far. Also, some of these agents have a decreased bioavailability or show some intrinsic toxicity, which also limits their working mitochondrial concentrations.
METHODS: By initially using PubMed specific queries for literature search, we review here cardiac mitochondrial effects of specific targeted and non-targeted antioxidants and pharmacological agents, including MitoE, MitoQ, MitoSNO, Mito-TEMPOL, SkQ1, SkQR1, carvedilol, trimetazidine, ranolazine, diazoxide and propofol.
RESULTS: The present review emphasizes new mitochondrial-targeting strategies which have emerged to address difficulties arising from current approaches. We also describe the strengths and weaknesses of these cardioprotective approaches.
CONCLUSION: Although effective therapies to target mitochondria in the context of CVDs are not under widespread clinical use, the new strategies proposed constitute a real promise for the development of therapies which may effectively prevent CVDs in the near future.
(Less)
- author
- Silva, Filomena S G ; Simoes, Rui F LU ; Couto, Renata and Oliveira, Paulo J
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- keywords
- Animals, Antioxidants/chemistry, Cardiotonic Agents/chemistry, Cardiovascular Diseases/drug therapy, Humans, Mitochondria/drug effects
- in
- Current Pharmaceutical Design
- volume
- 22
- issue
- 37
- pages
- 5698 - 5717
- publisher
- Bentham Science Publishers
- external identifiers
-
- scopus:85006060210
- pmid:27549376
- ISSN
- 1381-6128
- DOI
- 10.2174/1381612822666160822150243
- language
- English
- LU publication?
- no
- id
- 9b2aa1bc-cd76-4ea9-bd85-d6ef8207f0d2
- date added to LUP
- 2021-09-21 19:25:44
- date last changed
- 2024-06-30 20:35:50
@article{9b2aa1bc-cd76-4ea9-bd85-d6ef8207f0d2,
abstract = {{<p>BACKGROUND: Cardiovascular diseases (CVDs) are one of the main factors responsible for human morbidity and mortality. Since mitochondria play a critical role in the regulation of cardiac tissue homeostasis, this organelle is a critical target for the protective effects of several pharmaceuticals. Although specific mitochondria-targeted antioxidants and some pharmacological agents are described as potential cardioprotective agents, there are still a few effective mitochondrial therapies for the treatment of CVDs. Agents which have potential cardioprotective effects by directly targeting mitochondria in vitro and in vivo are still in pre-clinical or clinical trials, hence their widespread use in the clinic is still far. Also, some of these agents have a decreased bioavailability or show some intrinsic toxicity, which also limits their working mitochondrial concentrations.</p><p>METHODS: By initially using PubMed specific queries for literature search, we review here cardiac mitochondrial effects of specific targeted and non-targeted antioxidants and pharmacological agents, including MitoE, MitoQ, MitoSNO, Mito-TEMPOL, SkQ1, SkQR1, carvedilol, trimetazidine, ranolazine, diazoxide and propofol.</p><p>RESULTS: The present review emphasizes new mitochondrial-targeting strategies which have emerged to address difficulties arising from current approaches. We also describe the strengths and weaknesses of these cardioprotective approaches.</p><p>CONCLUSION: Although effective therapies to target mitochondria in the context of CVDs are not under widespread clinical use, the new strategies proposed constitute a real promise for the development of therapies which may effectively prevent CVDs in the near future.</p>}},
author = {{Silva, Filomena S G and Simoes, Rui F and Couto, Renata and Oliveira, Paulo J}},
issn = {{1381-6128}},
keywords = {{Animals; Antioxidants/chemistry; Cardiotonic Agents/chemistry; Cardiovascular Diseases/drug therapy; Humans; Mitochondria/drug effects}},
language = {{eng}},
number = {{37}},
pages = {{5698--5717}},
publisher = {{Bentham Science Publishers}},
series = {{Current Pharmaceutical Design}},
title = {{Targeting Mitochondria in Cardiovascular Diseases}},
url = {{http://dx.doi.org/10.2174/1381612822666160822150243}},
doi = {{10.2174/1381612822666160822150243}},
volume = {{22}},
year = {{2016}},
}