Journal Browser

Journal Browser

Biomarkers and Drug Targets for Longevity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 29 August 2024 | Viewed by 1299

Special Issue Editor

E-Mail Website
Guest Editor
1. Department of Preventive Cardiology and Lipidology, Chair of Nephrology and Hypertension, Medical University of Lodz, 93-338 Lodz, Poland
2. Ciccarone Center for the Prevention of Cardiovascular Disease, Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Interests: risk stratification; lipid-lowering therapy; drug development; atherosclerosis; cardiovascular prevention; epidemiology; meta-analyses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There has recently been high interest in all kinds of biomarkers and interventions that might help to evaluate expected lengths of lives and make it possible to extend lifetimes. This is especially important now, when in last several years, we have observed reductions in life expectancies by even over 2 years in some countries. On the one hand, our knowledge on the prediction of life expectancy seems to be increasingly accurate with the possibility of evaluating concrete biomarkers like telomere length, mitochondria activity and functions, changes in microvascular circulation, microbiome, advanced glycation end products, glycans, and whole-genome analysis. On the other hand, many inconsistencies remain in how to interpret these parameters correctly and, in particular, how they will be affected by concrete and dedicated interventions. This is currently the area of research undergoing the most development, but for most of these parameters, we still do not have clear results on whether they might indeed prolong our life.

As already identified in research, lifestyle factors such as a healthy diet and physical activity play a crucial role in healthy aging, the mechanisms of which mainly include modulating oxidative stress, metabolism, inflammation, genetic regulation, and cell signaling and survival. Lifestyle changes can have major effects on molecular biomarkers, mitochondrial activity, or white blood cell telomere length (LTL). This Special Issue will cover all molecular aspects of promoting longevity, aiming to provide further knowledge on new molecular targets, biomarkers, lifestyle improvement, and other interventions that might help to predict and improve the lifespan. This Special Issue invites submissions of original research and review articles.

Prof. Dr. Maciej Banach
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.


  • biomarkers
  • drug targets
  • genes
  • longevity
  • mitochondria
  • personalized interventions

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:


18 pages, 4896 KiB  
Antioxidant Efficacy of Hwangryunhaedok-tang through Nrf2 and AMPK Signaling Pathway against Neurological Disorders In Vivo and In Vitro
by Su-Jin Bae, Won-Yung Lee, Seon Been Bak, Seung Jin Lee, Su-Jin Hwang, Geun-Woo Kim, Byung-Soo Koo, Sun-Dong Park, Hye-Hyun Yoo, Choon-Ok Kim, Hyung Won Kang, Tae-Woo Oh and Young Woo Kim
Int. J. Mol. Sci. 2024, 25(4), 2313; https://doi.org/10.3390/ijms25042313 - 15 Feb 2024
Viewed by 1001
Alzheimer’s disease (AD) is a representative cause of dementia and is caused by neuronal loss, leading to the accumulation of aberrant neuritic plaques and the formation of neurofibrillary tangles. Oxidative stress is involved in the impaired clearance of amyloid beta (Aβ), and Aβ-induced [...] Read more.
Alzheimer’s disease (AD) is a representative cause of dementia and is caused by neuronal loss, leading to the accumulation of aberrant neuritic plaques and the formation of neurofibrillary tangles. Oxidative stress is involved in the impaired clearance of amyloid beta (Aβ), and Aβ-induced oxidative stress causes AD by inducing the formation of neurofibrillary tangles. Hwangryunhaedok-tang (HHT, Kracie K-09®), a traditional herbal medicine prescription, has shown therapeutic effects on various diseases. However, the studies of HHT as a potential treatment for AD are insufficient. Therefore, our study identified the neurological effects and mechanisms of HHT and its key bioactive compounds against Alzheimer’s disease in vivo and in vitro. In a 5xFAD mouse model, our study confirmed that HHT attenuated cognitive impairments in the Morris water maze (MWM) test and passive avoidance (PA) test. In addition, the prevention of neuron impairment, reduction in the protein levels of Aβ, and inhibition of cell apoptosis were confirmed with brain tissue staining. In HT-22 cells, HHT attenuates tBHP-induced cytotoxicity, ROS generation, and mitochondrial dysfunction. It was verified that HHT exerts a neuroprotective effect by activating signaling pathways interacting with Nrf2, such as MAPK/ERK, PI3K/Akt, and LKB1/AMPK. Among the components, baicalein, a bioavailable compound of HHT, exhibited neuroprotective properties and activated the Akt, AMPK, and Nrf2/HO-1 pathways. Our findings indicate a mechanism for HHT and its major bioavailable compounds to treat and prevent AD and suggest its potential. Full article
(This article belongs to the Special Issue Biomarkers and Drug Targets for Longevity)
Show Figures

Figure 1

Back to TopTop