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Biomolecules
Special Issues
Bioactive Compounds as Modifiers of Mitochondrial Function
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Bioactive Compounds as Modifiers of Mitochondrial Function

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Natural and Bio-derived Molecules".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 2991

Special Issue Editor

Dr. Mihail "Mike" Mitov

E-Mail Website
Guest Editor
Department of Physiology & Pharmacology, Sam Houston State University College of Osteopathic Medicine, 925 City Central Ave., Conroe, TX 77304, USA
Interests: cellular bioenergetics; redox biology; oxidative stress; thermobiology; muscle physiology; cancer pathophysiology; metabolic syndrome; neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Mitochondria is an organelle found in most eukaryotic cells, with a primary function of generating energy in the form of adenosine triphosphate (ATP). In addition to producing energy, mitochondria functions include storing calcium for cell signaling activities, generating heat when needed, and mediating cell growth and death. Bioactive compounds (broadly defined as natural, artificial, or synthesized compounds) could exhibit actions in the human body that may promote or improve health. Bioactive compounds have been studied and used since ancient times for their potential role in reducing illnesses, infections, cancer, diabetes, heart failure, Alzheimer and other diseases. In this Special Issue, we invite you to submit your original manuscripts, reviews, and special communications focusing on mitochondrial aspects of bioactive compound effects in the context of human or animal pathophysiology, pharmacology, and general health.

Dr. Mihail "Mike" Mitov
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • natural bioactive compounds
  • synthesized bioactive compounds
  • mitochondrial function
  • electron transport chain (ETC)
  • ATP production rate
  • oxygen consumption rate (OCR)
  • extracellular acidification rate (ECAR)

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Published Papers (2 papers)

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Research

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24 pages, 3969 KB  
Article
Kynurenic Acid Protects Against Myocardial Ischemia/Reperfusion Injury by Activating GPR35 Receptors and Preserving Mitochondrial Structure and Function
by Dóra Nógrádi-Halmi, Barbara Erdélyi-Furka, Dóra Csóré, Éva Plechl, Nóra Igaz, László Juhász, Marietta Zita Poles, Bernát Nógrádi, Roland Patai, Tamás Ferenc Polgár, Mónika Kiricsi, László Vécsei, Renáta Gáspár and Tamás Csont
Biomolecules 2025, 15(10), 1481; https://doi.org/10.3390/biom15101481 - 21 Oct 2025
Viewed by 276
Abstract
Acute myocardial infarction, often associated with ischemia/reperfusion injury (I/R), is a major healthcare issue ranking among the leading causes of death globally. Although kynurenic acid (KYNA), an endogenous tryptophan metabolite, has been previously shown to protect the cardiac tissue against I/R injury, its [...] Read more.
Acute myocardial infarction, often associated with ischemia/reperfusion injury (I/R), is a major healthcare issue ranking among the leading causes of death globally. Although kynurenic acid (KYNA), an endogenous tryptophan metabolite, has been previously shown to protect the cardiac tissue against I/R injury, its mechanism of action remains unclear. Therefore, here, we examined whether KYNA administration rescues H9c2 cardiac cells exposed to I/R through the preservation of the structural and functional integrity of the mitochondria. In addition, we assessed whether KYNA-derived agonism on G-protein coupled receptor 35 (GPR35) is involved in the protection of cardiac cells against simulated I/R (SI/R)-induced cellular demise. Our results demonstrated that KYNA attenuated the SI/R-induced calcium overload as well as impairments in the mitochondrial ultrastructure. Furthermore, administration of KYNA was shown to reduce mitochondrial superoxide production and preserve mitochondrial function in cells exposed to SI/R. Activation of the GPR35 receptors using an agonist other than KYNA rescued cardiac cells undergoing SI/R, attenuated the apoptotic activity, and improved various parameters of mitochondrial respiration. The administration of a synthetic GPR35 antagonist in parallel with KYNA attenuated the KYNA-induced cytoprotection. Our findings provide evidence that the protective effect of KYNA against SI/R-induced cardiac cell injury involves mitoprotective mechanisms, acting, at least in part, through the activation of GPR35 receptors. Full article
(This article belongs to the Special Issue Bioactive Compounds as Modifiers of Mitochondrial Function)
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Review

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29 pages, 2132 KB  
Review
Polyphenol-Based Therapeutic Strategies for Mitochondrial Dysfunction in Aging
by Tamara Maksimović, Carmen Gădău, Gabriela Antal, Mihaela Čoban, Oana Eșanu, Elisabeta Atyim, Alexandra Mioc and Codruța Șoica
Biomolecules 2025, 15(8), 1116; https://doi.org/10.3390/biom15081116 - 3 Aug 2025
Viewed by 1988
Abstract
Aging, a progressive and time-dependent decline in physiological functions, is driven by interconnected hallmarks, among which mitochondrial dysfunction plays a central role. Mitochondria not only regulate energy production but also play key roles in other cellular processes, including ROS generation, apoptosis, and metabolic [...] Read more.
Aging, a progressive and time-dependent decline in physiological functions, is driven by interconnected hallmarks, among which mitochondrial dysfunction plays a central role. Mitochondria not only regulate energy production but also play key roles in other cellular processes, including ROS generation, apoptosis, and metabolic signaling—all of which decline with aging. Polyphenols are a diverse group of natural compounds found in fruits, vegetables, tea, and wine; they emerged as promising anti-aging agents due to their ability to modulate several hallmarks of aging, particularly mitochondrial dysfunction. This review explores how various polyphenolic classes influence mitochondrial function and mitigate aging-related decline. These natural compounds have been shown to reduce oxidative stress, increase energy production, and help maintain normal mitochondrial structure. Moreover, in vitro and in vivo studies suggest that polyphenols can delay signs of aging and improve physical and cognitive functions. Overall, polyphenols show great potential to promote healthy aging and even delay the decline in physiological functions by protecting and enhancing mitochondrial health. Full article
(This article belongs to the Special Issue Bioactive Compounds as Modifiers of Mitochondrial Function)
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