Amyotrophic lateral sclerosis (ALS) is a fast progressing neurodegenerative disease leading to quadriplegia, anarthria and respiratory insufficiency. A large variety of phenotypes and disability progression requires individually tailored management. Identification of predictors of poor prognosis may not only improve management, but also allow for more precise patients’ stratification for clinical trials or research studies. The aim of the study was to investigate the influence of emotional lability present at disease onset on ALS progression by exploring its direct impact on the decay of the ALS Functional Rating Scale-Revised (ALSFRS-R). The study was performed in a group of 1145 patients from Germany, Poland, Portugal and Turkey between 2014 and 2018. The analysis showed that the presence of emotional lability at ALS onset was linked to a faster decline of ALSFRS-R (0.70 vs 0.50, p<0.0001), in case of either bulbar (0.80 vs 0.65, p<0.05) or limb disease onset (0.59 vs 0.46, p <0.01). It was most prominent in the bulbar subscore of ALSFRS-R. A multiple regression analysis showed a direct influence of emotional lability at ALS onset on disease progression, regardless of age, gender, site of onset, weight loss, cognitive impairment and diagnosis delay (β=0.071; p=0.019). It can therefore be concluded that the presence of emotional lability at the disease onset is an independent factor of faster disease progression in ALS.

Emerging evidence indicates that the intestinal microbiota could interact with the central nervous system and modulate multiple pathophysiological changes, including the integrity of intestinal barrier and blood-brain barrier, as well as neuroinflammatory response. In the present study, we investigated the potential role of intestinal microbiota in the pathophysiological process of postoperative cognitive dysfunction. Six-month-old APP/PS1 mice were subjected to partial hepatectomy to establish surgery model and exhibited cognitive dysfunction. The expressions of inflammatory mediators increased and tight junction proteins (ZO-1 and Occludin) levels decreased in the intestine and hippocampus. The 16S ribosomal RNA gene sequencing showed altered β diversity and intestinal microbiota richness after surgery, including genus Rodentibacter, Bacteroides, Ruminococcaceae_UCG_014 and Faecalibaculum, as well as family Eggerthellaceae and Muribaculaceae. Furthermore, prebiotics (Xylooligosaccharides, XOS) intervention effectively attenuated surgery-induced cognitive dysfunction and intestinal microbiota alteration, reduced inflammatory responses, and improved the integrity of tight junction barrier in the intestine and hippocampus. In summary, the present study indicates that intestinal microbiota alteration, the related intestinal barrier and blood-brain barrier damage, and inflammatory responses participate the pathophysiological process of postoperative cognitive dysfunction. Prebiotics intervention could be a potential preventative approach.

Understanding how blood lipid levels change with age in the general population is a precondition to defining dyslipidemia. To explore age-related trends in LDL-C and non-HDL-C levels in the general population, a large-scale cross-sectional study with 49,201 males and 35,084 females was adopted. Trends of non-HDL-C and LDL-C levels were plotted against each age (18 to 85 years old, one-year increments); the trends, as well as the influence of confounding factors on the trends, were validated and adjusted by linear regression modeling. The trajectory of LDL-C and non-HDL-C levels by age displayed a nonlinear correlation trend. Further multivariate linear regression modeling that incorporated sex-specific age phases showed that age was positively associated with LDL-C and non-HDL-C levels, with coefficients of 0.018 and 0.031, respectively, in females aged ≥18 to ≤56 years and negatively associated with LDL-C and non-HDL-C levels, with coefficients of -0·013 and -0.015, respectively, in females aged ≥57 years. The LDL-C and non-HDL-C levels increased with age in males ≥18 to ≤33 years of age, with coefficients of 0.025 and 0.053, respectively; the lipid levels plateaued at ≥34 to ≤56 years of age and subsequently decreased in those ≥57 years of age, with coefficients of -0.008 and -0.018, respectively. In contrast, pooled analyses without age stratification concealed these details. In conclusion, fluctuating increasing and decreasing lipid levels occurred with phases of aging in both sexes. Well-grounded age stratification is necessary to improve lipid-related pathophysiological studies.

The switch between osteogenic and adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) plays a key role in aging-induced osteoporosis. In this study, miR-19a-3p was obviously downregulated in BMSCs from aged humans and mice. Overexpressed miR-19a-3p evidently reduced aging-induced bone loss in mice and promoted osteogenic differentiation of BMSCs, while silenced miR-19a-3p manifestly increased aging-induced bone loss in mice and repressed osteogenic differentiation of BMSCs. Hoxa5 was significantly downregulated in the BMSCs from aged mice and contribute to miR-19a-3p-induced osteoblast differentiation as a direct target gene of miR-19a-3p. Furthermore, lncRNA Xist was found as a sponge of miR-19a-3p to repress BMSCs osteogenic differentiation. In conclusion, our study reveals the critical role of the lncRNA Xist/miR-19a-3p/Hoxa5 pathway in aging-induced osteogenic differentiation of BMSCs, indicating the potential therapeutic target for osteoporosis.

Coronavirus disease 2019 (COVID-19) is a global pandemic associated with a high mortality. Our study aimed to determine the clinical risk factors associated with disease progression and prolonged viral shedding in patients with COVID-19. Consecutive 564 hospitalized patients with confirmed COVID-19 between January 17, 2020 and February 28, 2020 were included in this multicenter, retrospective study. The effects of clinical factors on disease progression and prolonged viral shedding were analyzed using logistic regression and Cox regression analyses. 69 patients (12.2%) developed severe or critical pneumonia, with a higher incidence in the elderly and in individuals with underlying comorbidities, fever, dyspnea, and laboratory and imaging abnormalities at admission. Multivariate logistic regression analysis indicated that older age (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.02-1.06), hypertension without receiving angiotensinogen converting enzyme inhibitors or angiotensin receptor blockers (ACEI/ARB) therapy (OR, 2.29; 95% CI, 1.14-4.59), and chronic obstructive pulmonary disease (OR, 7.55; 95% CI, 2.44-23.39) were independent risk factors for progression to severe or critical pneumonia. Hypertensive patients without receiving ACEI/ARB therapy showed higher lactate dehydrogenase levels and computed tomography (CT) lung scores at about 3 days after admission than those on ACEI/ARB therapy. Multivariate Cox regression analysis revealed that male gender (hazard ratio [HR], 1.22; 95% CI, 1.02-1.46), receiving lopinavir/ritonavir treatment within 7 days from illness onset (HR, 0.75; 95% CI, 0.63-0.90), and receiving systemic glucocorticoid therapy (HR, 1.79; 95% CI, 1.46-2.21) were independent factors associated with prolonged viral shedding. Our findings presented several potential clinical factors associated with developing severe or critical pneumonia and prolonged viral shedding, which may provide a rationale for clinicians in medical resource allocation and early intervention.

The focus of our investigation was to determine the feasibility of using six visual rating scales as whole-brain imaging markers for monitoring atrophied brain volume in Parkinson’s disease (PD). This was a prospective cross-sectional single-center observational study. A total of 98 PD patients were enrolled and underwent an MRI scan and a battery of neuropsychological evaluations. The brain volume was calculated using the online resource MRICloud. Brain atrophy was rated based on six visual rating scales. Correlation analysis was performed between visual rating scores and brain volume and clinical features. We found a significant negative correlation between the total scores of visual rating scores and quantitative brain volume, indicating that six visual rating scales reliably reflect whole brain atrophy in PD. Multiple linear regression-based analyses indicated severer non-motor symptoms were significantly associated with higher scores on the visual rating scales. Furthermore, we performed sample size calculations to evaluate the superiority of visual rating scales; the result show that using total scores of visual rating scales as an outcome measure, sample sizes for differentiating cognition injury require significantly fewer subjects (n = 177) compared with using total brain volume (n = 2524). Our data support the use of the total visual rating scores rather than quantitative brain volume as a biomarker for monitoring cerebral atrophy.

Aging is a major risk factor for the development of osteoarthritis (OA). One hallmark of aging is loss of proteostasis resulting in increased cellular stress and cell death. However, its effect on the development of OA is not clear. Here, using knee articular cartilage tissue from young and old cynomolgus monkeys (Macaca fascicularis), we demonstrate that with aging there is loss of molecular chaperone expression resulting in endoplasmic reticulum (ER) stress and cell death. Chondrocytes from aged articular cartilage showed decreased expression of molecular chaperones, including protein disulfide isomerase, calnexin, and Ero1-like protein alpha, and increased immunohistochemical staining for ER stress markers (phosphorylated IRE1 alpha, spliced X-box binding protein-1, activating transcription factor 4 and C/EBP homologous protein), and apoptotic markers [cleaved caspase 3 and cleaved poly(ADP-ribose) polymerase], suggesting that decreased expression of molecular chaperone during aging induces ER stress and chondrocyte apoptosis in monkey articular cartilage. Apoptosis induced by aging-associated ER stress was further confirmed by TUNEL staining. Aged monkey cartilage also showed increased expression of nuclear protein 1 (Nupr1) and tribbles related protein-3 (TRB3), known regulators of apoptosis and cell survival pathways. Treatment of cultured monkey chondrocytes with a small molecule chemical chaperone, 4-phenylbutyric acid (PBA, a general ER stress inhibitor) or PERK Inhibitor I (an ER stress inhibitor specifically targeting the PERK branch of the unfolded protein response pathway), decreased the expression of ER stress and apoptotic markers and reduced the expression of Nupr1 and TRB3. Consistent with the above finding, knockdown of calnexin expression induces ER stress and apoptotic markers in normal human chondrocytes in vitro. Taken together, our study clearly demonstrates that aging promotes loss of proteostasis and induces ER stress and chondrocyte apoptosis in articular cartilage. Thus, restoring proteostasis using chemical/molecular chaperone or ER stress inhibitor could be a therapeutic option to treat aged-linked OA.

Circulating factors associated with aging have been shown to be involved in the development of age-related chronic and acute brain diseases. Here, we aimed to investigate the roles and mechanisms of CCL12, a circulating factor that is highly expressed in the plasma of aged rodents after intracerebral hemorrhage (ICH) using parabiosis and ICH models. Neurological deficit score (NDS), mortality rate, brain water content (BWC), and levels of inflammatory factors were determined to assess the degree of ICH-induced brain injury. Peripheral inflammatory cell infiltration was examined using immunofluorescence and flow cytometry. After confirming that acute brain injury after ICH was aggravated with age, we found that brain and plasma CCL12 levels were markedly higher in old mice than in young mice after ICH, and that plasma CCL12 was able to enter the brain. Using CCL12^-/- mice, we showed that the degree of damage in the brain—as determined by NDS, mortality rate, BWC, levels of inflammatory factors, and numbers of degenerative and apoptotic neural cells and surviving neurons was significantly attenuated compared to that observed in old wild-type (WT) mice. These effects were reversed in CCL12-treated old mice. The detrimental effects caused by CCL12 may involve its ability to recruit macrophages and T cells. Finally, the administration of an anti-CCL12 antibody markedly improved the outcomes of ICH mice. Our results are the first to indicate that elevated peripheral CCL12 levels in old mice aggravates ICH-induced brain injury by recruiting macrophages and T cells. Thus, CCL12 may be a new target for ICH treatment.

Adipose-derived stem cells (ASCs) are highly chondrogenic and can be used to treat knee osteoarthritis (KOA) by alleviating cartilage defects. Acupotomy, a biomechanical therapy guided by traditional Chinese medicine theory, alleviates cartilage degradation and is widely used in the clinic to treat KOA by correcting abnormal mechanics. However, whether combining acupotomy with ASCs will reverse cartilage degeneration by promoting chondrocyte proliferation in KOA rabbits is unknown. The present study aimed to investigate the effects of combination therapy of acupotomy and ASCs on chondrocyte proliferation and to determine the underlying mechanism in rabbits with KOA induced by knee joint immobilization for 6 weeks. After KOA modeling, five groups of rabbits (acupotomy, ASCs, acupotomy + ASCs, model and control groups) received the indicated intervention for 4 weeks. The combination therapy significantly restored the KOA-induced decrease in passive range of motion (PROM) in the knee joint and reduced the elevated serum level of cartilage oligomeric matrix protein (COMP), a marker for cartilage degeneration. Furthermore, magnetic resonance imaging (MRI) and scanning electron microscopy (SEM) images showed that the combination therapy inhibited cartilage injury. The combination therapy also significantly blocked increases in the mRNA and protein expression of glycogen synthase kinase-3β (GSK3β) and decreases in the mRNA and protein expression of cyclin D1/CDK4 and cyclin D1/CDK6 in cartilage. These findings indicated that the combination therapy mitigated knee joint immobility, promoted chondrocyte proliferation and alleviated cartilage degeneration in KOA rabbits, and these effects may be mediated by specifically regulating the GSK3β-cyclin D1-CDK4/CDK6 pathway.

Postoperative cognitive dysfunction (POCD) is a significant clinical issue. Aging is a risk factor for POCD. It is known that not every patient develops POCD. This situation shall be similar in animals. Determination of POCD is individual-based in humans but group-based in animal studies. This difference prevents effective evaluation of biomarkers and interventions for POCD in preclinical studies. The objective of this study was to determine whether individual animal could be assessed for POCD by a system similar to that for patients. Seven-week old CD1 and 18-month old C57BL/6 male mice were subjected to right carotid arterial exposure under isoflurane anesthesia. Mice were evaluated by Barnes maze and fear conditioning either post-surgery alone or both prior to surgery and post-surgery. Surgery increased the time to identify the target box in Barnes maze when tested one day or 8 days after the training sessions and reduced freezing behavior in fear conditioning test. This phenomenon occurred in 7-week old animals with and without evaluation before the surgery and in 18-month old mice evaluated before and after surgery. Based on the method and criteria used for a human whose cognition was evaluated before and after surgery to assess individual decline of cognition, 7 in 21 mice in the surgical group and 1 in 21 mice in control group of 7-week old mice had cognitive dysfunction. Among 18-month old mice, 13 in 21 mice in the surgical group and 2 in 20 mice in the control group had cognitive dysfunction. The incidence of cognitive dysfunction in mice with surgery was higher than that in control mice no matter whether young adult (P = 0.045) or old mice (P < 0.001) were considered. These results indicate that surgery induces POCD in mice. Individual animal-based assessment can be used to identify animals with POCD.

Recent studies have revealed novel forms of cell death beyond the canonical types of cellular apoptosis and necrosis, and these novel forms of cell death are induced by extreme microenvironmental factors. Pyroptosis, a type of regulated cell death, occurs when pattern recognition receptors (PRRs) induce the activation of cysteine-aspartic protease 1 (caspase-1) or caspase-11, which can trigger the release of the pyrogenic cytokines interleukin-1β (IL-1β) and IL-18. Osteoarthritis (OA), the most common joint disease worldwide, is characterized by low-grade inflammation and increased levels of cytokines, including IL-1β and IL-18. Additionally, some damaged chondrocytes associated with OA exhibit morphological changes consistent with pyroptosis, suggesting that this form of regulated cell death may contribute significantly to the pathology of OA. This review summarizes the molecular mechanisms of pyroptosis and shows the critical role of NLRP3 (NLR family, pyrin domain containing 3; NLR refers to “nucleotide-binding domain, leucine-rich repeat”) inflammasomes. We also provide evidence describing potential role of pyroptosis in OA, including the relationship with OA risk factors and the contribution to cartilage degradation, synovitis and OA pain.

Myocardial fibrosis is observed in various cardiovascular diseases and plays a key role in the impairment of cardiac function. Endomyocardial biopsy, as the gold standard for the diagnosis of myocardial fibrosis, has limitations in terms of clinical application. Therefore, biomarkers have been recommended for noninvasive assessment of myocardial fibrosis. This review discusses the role of biomarkers in myocardial fibrosis from the perspective of collagen.

The COVID-19 patients were first detected in China, in December 2019, then the novel virus with associated pneumonia and other diseases spread quickly to worldwide becoming a serious public health intimidation. Despite all the efforts, the pharmacological agents used for controlling or treating the disease, especially respiratory problems, have not been accomplished so far. Among various treatment options, mesenchymal stem cell-based cellular therapies are being investigated, because of their regeneration ability and multipotency along with other features like immunomodulation, antifibrosis and anti-inflammatory effects. This paper intends to analyze the current clinical trials on stem cell treatment of novel virus, searching and reviewing the available information and the International Clinical Trials Registry Platform (ICTRP) of World Health Organization (WHO). We concluded that the stem cell treatment of COVID-19 is found promising with pilot studies’ results, but still in the early development phase. There is an urgent need for large-scale investigations to confirm and validate the safety and efficacy profile of these therapies with reliable scientific evidence.

Mesenchymal Stem Cells (MSCs), and Adipose-Derived Mesenchymal Stem Cells (AD-MSCs) have been used for many years in regenerative medicine for clinical and surgical applications. Additionally, recent studies reported improved respiratory activity after intravenous administration of MSCs into patients affected by coronavirus disease 2019 (COVID-19) caused by the Coronavirus 2 (SARS-CoV-2) suggesting their role as anti-viral therapy. Severe COVID-19 patients usually progress to acute respiratory distress syndrome, sepsis, metabolic acidosis that is difficult to correct, coagulation dysfunction, multiple organ failure, and even death in a short period after onset. Currently, there is still a lack of clinically effective drugs for such patients. The high secretory activity, the immune-modulatory effect, and the homing ability make MSCs and in particular AD-MSCs both a potential tool for the anti-viral drug-delivery in the virus microenvironment and potential cellular therapy. AD-MSCs as the most important exponent of MSCs are expected to reduce the risk of complications and death of patients due to their strong anti-inflammatory and immune-modulatory capabilities, which can improve microenvironment, promote neovascularization and enhance tissue repair capabilities. In this literature review, the role of regenerative strategies through MSCs, AD-MSCs, and adipocyte-secreted exosomal microRNAs (A-SE-miRs) as a potential antiviral therapy was reported, comparing the results found with current research progress on drugs and vaccines in COVID-19 disease.

Erectile dysfunction (ED) is a common sexual disorder in adult males and one of the most important factors affecting their quality of life and that of their partners. Although PDE5 inhibitors (PDE5is) are the first choice for improving erectile function, there is a substantial proportion of ED patients, termed PDE5i nonresponders, who do not respond to PDE5is. Because of the lack of effective therapies, these patients always have serious social and psychological problems due to ED, which should be addressed. Here, we review the available literature about ED and PDE5is and propose several strategies for mitigating ED in PDE5i nonresponders.

Epigenetics has been recognized to play an important role in physiological and pathological processes of the human body. Accumulating evidence has indicated that epigenetic mechanisms contribute to the pathogenesis of age-related macular degeneration (AMD). Although the susceptibility related to genetic variants has been revealed by genome-wide association studies, those genetic variants may predict AMD risk only in certain human populations. Other mechanisms, particularly those involving epigenetic factors, may play an important role in the pathogenesis of AMD. Therefore, we briefly summarize the most recent reports related to such epigenetic mechanisms, including DNA methylation, histone modification, and non-coding RNA, and the interplay of genetic and epigenetic factors in the pathogenesis of AMD.

Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide and causes severe financial and social burdens. Despite much research on the pathogenesis of AD, the neuropathological mechanisms remain obscure and current treatments have proven ineffective. In the past decades, transgenic rodent models have been used to try to unravel this disease, which is crucial for early diagnosis and the assessment of disease-modifying compounds. In this review, we focus on transgenic rodent models used to study amyloid-beta pathology in AD. We also discuss their possible use as promising tools for AD research. There is still no effective treatment for AD and the development of potent therapeutics are urgently needed. Many molecular pathways are susceptible to AD, ranging from neuroinflammation, immune response, and neuroplasticity to neurotrophic factors. Studying these pathways may shed light on AD pathophysiology as well as provide potential targets for the development of more effective treatments. This review discusses the advantages and limitations of these models and their potential therapeutic implications for AD.

Mitochondria are classically known to be cellular energy producers. Given the high-energy demanding nature of neurons in the brain, it is essential that the mitochondrial pool remains healthy and provides a continuous and efficient supply of energy. However, mitochondrial dysfunction is inevitable in aging and neurodegenerative diseases. In Alzheimer’s disease (AD), neurons experience unbalanced homeostasis like damaged mitochondrial biogenesis and defective mitophagy, with the latter promoting the disease-defining amyloid β (Aβ) and p-Tau pathologies impaired mitophagy contributes to inflammation and the aggregation of Aβ and p-Tau-containing neurotoxic proteins. Interventions that restore defective mitophagy may, therefore, alleviate AD symptoms, pointing out the possibility of a novel therapy. This review aims to illustrate mitochondrial biology with a focus on mitophagy and propose strategies to treat AD while maintaining mitochondrial homeostasis.

Frailty is increasingly recognized as a better predictor of adverse postoperative events than chronological age. The objective of this review was to systematically evaluate the effect of frailty on postoperative morbidity and mortality. Studies were included if patients underwent non-cardiac surgery and if frailty was measured by a validated instrument using physical, cognitive and functional domains. A systematic search was performed using EMBASE, MEDLINE, Web of Science, CENTRAL and PubMed from 1990 - 2017. Methodological quality was assessed using an assessment tool for prognosis studies. Outcomes were 30-day mortality and complications, one-year mortality, postoperative delirium and discharge location. Meta-analyses using random effect models were performed and presented as pooled risk ratios with confidence intervals and prediction intervals. We included 56 studies involving 1.106.653 patients. Eleven frailty assessment tools were used. Frailty increases risk of 30-day mortality (31 studies, 673.387 patients, risk ratio 3.71 [95% CI 2.89-4.77] (PI 1.38-9.97; I2=95%) and 30-day complications (37 studies, 627.991 patients, RR 2.39 [95% CI 2.02-2.83). Risk of 1-year mortality was threefold higher (six studies, 341.769 patients, RR 3.40 [95% CI 2.42-4.77]). Four studies (N=438) reported on postoperative delirium. Meta-analysis showed a significant increased risk (RR 2.13 [95% CI 1.23-3.67). Finally, frail patients had a higher risk of institutionalization (10 studies, RR 2.30 [95% CI 1.81- 2.92]). Frailty is strongly associated with risk of postoperative complications, delirium, institutionalization and mortality. Preoperative assessment of frailty can be used as a tool for patients and doctors to decide who benefits from surgery and who doesn’t.

Besides extracellular deposition of amyloid beta and formation of phosphorylated tau in the brains of patients with Alzheimer’s disease (AD), the pathogenesis of AD is also thought to involve mitochondrial dysfunctions and altered neurotransmission systems. However, none of these components can describe the diverse cognitive, behavioural, and psychiatric symptoms of AD without the pathologies interacting with one another. The purpose of this review is to understand the relationships between mitochondrial and neurotransmission dysfunctions in terms of (1) how mitochondrial alterations affect cholinergic and monoaminergic systems via disruption of energy metabolism, oxidative stress, and apoptosis; and (2) how different neurotransmission systems drive mitochondrial dysfunction via increasing amyloid beta internalisation, oxidative stress, disruption of mitochondrial permeabilisation, and mitochondrial trafficking. All these interactions are separately discussed in terms of neurotransmission systems. The association of mitochondrial dysfunctions with alterations in dopamine, norepinephrine, and histamine is the prospective goal in this research field. By unfolding the complex interactions surrounding mitochondrial dysfunction in AD, we can better develop potential treatments to delay, prevent, or cure this devastating disease.

Osteoarthritis is the most prevalent arthritis typically characterized by degradation of cartilage. However, its pathogenesis is not fully understood. Currently, osteoarthritis is best considered a disease of the whole “joint organ”. Infrapatellar fat pad (IFP), an adipose tissue near synovium, is now attaching importance to researchers for its inflammatory phenotype. In this narrative review, a large body of evidence has been gathered for the involvement of IFP in the development of knee osteoarthritis. Additionally, the underlying mechanisms of how IFP can be involved in this process have been proposed. However, further investigations are needed to better understand its precise role in this process and its underlying mechanism, and beyond that, to develop new strategies to slow down the degenerative process and explore an effective and timely diagnosis of the disease.

Aging is a common risk factor for the occurrence and development of many diseases, such as Parkinson’s disease, Alzheimer’s disease, diabetes, hypertension, atherosclerosis and coronary heart disease, and cancer, among others, and is a key problem threatening the health and life expectancy of the elderly. Oxidative damage is an important mechanism involved in aging. The latest discovery pertaining to oxidative damage is that 8-oxoGsn (8-oxo-7,8-dihydroguanosine), an oxidative damage product of RNA, can represent the level of oxidative stress. The significance of RNA oxidative damage to aging has not been fully explained, but the relationship between the accumulation of 8-oxoGsn, a marker of RNA oxidative damage, and the occurrence of diseases has been confirmed in many aging-related diseases. Studying the aging mechanism, monitoring the aging level of the body and exploring the corresponding countermeasures are of great significance for achieving healthy aging and promoting public health and social development. This article reviews the progress of research on 8-oxoGsn in aging-related diseases.