Interventions to Delay or Even Reverse Aging: A Comprehensive Analysis of Aging Mechanisms and Strategies

Interventions to Delay or Even Reverse Aging: A Comprehensive Analysis of Aging Mechanisms and Strategies

What is aging? Faced with the growing trend of population aging, what can we do?
Recently, more than 20 institutions of higher learning, including Tsinghua University, Peking University, and the Chinese Academy of Sciences, jointly published a comprehensive review on aging research titled The Landscape of Aging—one of the most detailed international reviews on aging to date. To make this valuable research more accessible, this article provides a simplified, easy-to-read version of the review, focusing on three key topics:
  1. How the human body gradually ages;
  2. What changes occur in organs, tissues, and systems during aging;
  3. What effective anti-aging interventions are currently available.

Figure: Landscape of Aging

Key elements: Mechanisms of aging (genomic instability, epigenetic alterations, telomere attrition, etc.); organ/system aging (circulatory system, nervous system, hematopoietic system, bones, reproductive system, gut microbiota, etc.); anti-aging interventions (anti-aging drugs, gene therapy, stem cell therapy, novel technologies like AI-aided drug discovery, single-cell omics, etc.).

Part 1: Molecular Mechanisms of Aging

The academic community believes that cellular senescence impairs tissue function and regenerative capacity, leading to age-related diseases. Thus, many hallmarks of human aging are associated with cellular senescence[1].
During aging, accumulated DNA damage—modified by epigenetic changes, autophagic dysfunction, and metabolic disorders—induces the senescence-associated secretory phenotype (SASP)[2]. These molecular changes also trigger mechanisms such as telomere shortening and mitochondrial dysfunction[3]. Ultimately, all these aging-related molecular mechanisms lead to stem cell dysfunction and exhaustion[4].
Below is a breakdown of the key molecular mechanisms of aging:

1. Regulation of Aging by Genomic Stability

  • Healthy state: Genomic stability is maintained through DNA repair, reduced inflammation, and tissue renewal. Long-lived models (e.g., naked mole-rats, beavers, whales, bats) and radiation-resistant organisms (e.g., tardigrades, Deinococcus radiodurans) exhibit strong genomic stability.
  • Aging state: Genomic instability (e.g., activated retrotransposons, impaired DNA repair, accumulated DNA damage) triggers chronic inflammation and age-related diseases. Short-lived models, mice with gene knockouts, and patients with progeroid syndromes often show reduced genomic stability.
  • Interventions: Senolytics (drugs that clear senescent cells), senomorphics (drugs that suppress SASP), DNA repair activators, and nucleoside reverse transcriptase inhibitors (NRTIs, which inhibit retrotransposons) can help stabilize the genome.

2. SASP Promotes Cellular Senescence

Genotoxic stress induces structural changes in chromatin (e.g., reduced Lamin B1), accumulation of dysfunctional mitochondria, and DNA breaks. These events activate the DNA damage response (DDR) via the MRN complex, upregulating senescence markers such as p16<sup>INK4a</sup>, p21<sup>CIP1</sup>, and senescence-associated β-galactosidase (SA-β-Gal).
Subsequently,:
  • Reactive oxygen species (ROS) accumulate in the cytoplasm, enhancing ribosomal translation;
  • Damaged DNA (e.g., cytoplasmic chromatin fragments, CCFs) and HMGB1 (a nuclear protein) are released into the extracellular space;
  • The Golgi apparatus synthesizes and secretes SASP factors (e.g., cytokines IL-6/IL-8/IL-1α/IL-1β, matrix metalloproteinases MMPs, chemokines, and growth factors), further promoting cellular senescence.

3. Mitochondrial Function in Aging and Interventions

Aging is associated with declined mitochondrial biogenesis, disrupted mitochondrial dynamics (fission/fusion balance), and impaired quality control (e.g., reduced mitophagy and mitochondrial unfolded protein response, UPR<sup>mt</sup>).
Anti-aging interventions (exercise, dietary adjustments, drugs) can promote healthy aging by:
  • Enhancing mitochondrial biogenesis (via activating PGC-1α, a key regulator of mitochondrial synthesis);
  • Restoring mitochondrial dynamics (balancing fission and fusion);
  • Improving mitochondrial quality control (boosting mitophagy and UPR<sup>mt</sup>).

4. Metabolic Control of Aging via Signaling Pathways

Aging and longevity are metabolically regulated by the interplay of three key systems:
  1. Nutrient-sensing pathways: mTOR, AMPK, and Sirtuins (SIRT1–SIRT7);
  2. Hormonal signaling networks: Insulin/IGF-1 axis;
  3. Stress response pathways: Endoplasmic reticulum (ER) unfolded protein response (UPR<sup>ER</sup>).
For example:
  • High glucose or saturated fatty acids (SFAs) activate the insulin/IGF-1 axis (INSR/IGF1R → IRS1/2 → PI3K → AKT), which accelerates aging if overactivated;
  • Low energy levels (high AMP/ATP ratio) activate AMPK, which inhibits mTORC1, promotes autophagy, and extends healthspan;
  • SIRT1 (a member of the Sirtuin family) is activated by NAD+ and regulates glucose metabolism, lipid homeostasis, and DNA repair.

5. Telomere Attrition and Cellular Senescence

Telomeric DNA shortens gradually with each round of somatic cell replication, eventually triggering cellular senescence.
Factors accelerating telomere damage include:
  • Lifestyle (smoking, poor diet, lack of exercise);
  • Stress (psychological, physical, social);
  • Environment (pollutants, extreme climates);
  • Infections (viruses, bacteria, fungi).
Telomere protection relies on the shelterin complex (TRF1, TRF2, RAP1, TPP1, POT1, TIN2). When telomeres are damaged (e.g., oxidative stress, DNA damage), the shelterin complex is disrupted, leading to genomic instability, hormonal imbalance, inflammation, immune deficiency, metabolic disorders, and ultimately cellular senescence.

6. Stem Cell Senescence and Impaired Regeneration

Stem cell senescence is driven by multiple interconnected factors:
  • SASP (senescence-associated secretory phenotype);
  • Upregulation of senescence markers (p16, p21, SA-β-Gal);
  • Mitochondrial dysfunction and increased ROS;
  • DNA damage and epigenetic alterations;
  • Autophagic and metabolic disorders.
These changes impair stem cell self-renewal capacity, reducing tissue regeneration and accelerating aging.
In summary, aging-related mechanisms do not act in isolation—they interact synergistically to induce systemic aging.

Part 2: Aging Characteristics of Human Organs

Driven by the above aging mechanisms, different organs, tissues, and systems in the human body age at varying rates. Below are key aging features of major organs and targeted interventions:

1. Heart

  • Aging features: Cardiac fibroblasts proliferate with age, leading to collagen accumulation, cardiac fibrosis, and impaired heart function. Additionally, disrupted protein homeostasis and mitochondrial dysfunction in cardiomyocytes further accelerate cardiac aging[7].
  • Interventions:
    • Antioxidant peptides (targeting mitochondrial dysfunction);
    • Caloric restriction (reducing fibrosis);
    • Small-molecule compounds, anti-aging drugs, stem cell therapy;
    • Various forms of exercise (e.g., aerobic exercise, resistance training).

2. Blood Vessels

  • Aging features: Elastic fiber fragmentation and collagen deposition in blood vessels widen the vascular lumen. Telomere attrition, abnormal expression of senescence markers (p53, p21, p16, ROS), and SASP-related genes increase vascular stiffness and reduce responsiveness to internal/external stimuli[9].
  • Interventions:
    • Small-molecule compounds (NMN, NR, metformin, resveratrol, spermidine);
    • Senolytics (clearing senescent vascular cells);
    • Stem cell therapy.
Figure: Vascular Aging and InterventionsLeft: Factors promoting vascular aging (genetic mutations, replicative stress, shear stress, cardiovascular disease); Right: Protective factors (protective genetic variations, small molecules like metformin, fresh blood infusion, stem cell therapy, caloric restriction, physical activity).

3. Reproductive System

  • Female reproductive aging: Manifested as endocrine disorders and increased risk of metabolic diseases.
    • Interventions: Senotherapy (most promising for female reproductive aging); melatonin; mitochondrial replacement therapy; nuclear genome transfer; autologous germline mitochondrial energy transfer (AUGMENT) (undergoing clinical safety evaluation)[12].
  • Male reproductive aging: Characterized by declining fertility with age[11].
    • Interventions: Oral antioxidants (vitamin C, vitamin E, vitamin D, selenium, folic acid, zinc, carnitine); anti-aging supplements/drugs (melatonin, quercetin, resveratrol); testosterone replacement therapy (common clinical practice)[13].

Part 3: Effective Anti-Aging Interventions

"From the moment of birth, humans begin the countdown to aging and death." While aging is an inevitable physiological process in nature, decades of research and clinical practice have identified numerous strategies to prevent or intervene in age-related diseases and extend healthspan.

1. Anti-Aging Substances

Clinical studies are ongoing to screen effective anti-aging substances, with key categories listed below:
Category Targets Example Drugs/Supplements
Senolytics Bcl-2/Bcl-xl, HSP90, Na+/K+ ATPase, FOXO4-p53, MDM2-p53, SA-β-Gal ABT-263[14], 17-DMAG[15], Digoxin[16], FOXO4-DRI[17], RG7112[17], SSK-1[17]
NAD+ Metabolic Modulators NAD+ synthesis, NAMPT, ACMSD, NAD+-consuming enzymes (CD38, SARM1) NR[18], NMN[18], NAM[18], P7C3[18], TES-991[18], 78c[18], Isoquinolines[18]
Sirtuin Activators SIRT1 Resveratrol[19]
IGF1 Signaling Inhibitors IGF1 Signaling Pathway Acarbose[20], Spermidine[20]
mTOR Inhibitors mTOR Pathway Rapamycin[21], Palomid 529[21]
AMPK Activators AMPK Pathway Metformin[22], Aspirin[22], α-KG[23], Berberine (BBR)[22]
Stem Cell Anti-Aging Agents Stem Cell Senescence (WRN deficiency, SASP, ROS) Vitamin C[24], WM-3835[24], Quercetin[24], Gallic Acid[24], Uridine[24]
  • Senolytics: Directly clear senescent cells to extend healthspan. ABT-263 was the first reported broad-spectrum senolytic, capable of clearing senescent cells and restoring the vitality of aged tissue stem cells[14]. Other senolytics (17-DMAG, digoxin, ouabain, FOXO4-DRI) also reverse cellular senescence[15-17].
  • NAD+ Boosters & Sirtuin Activators: NMN and NR (NAD+ precursors) safely and efficiently increase NAD+ levels[18]. Resveratrol (a histone deacetylase inhibitor) activates the longevity gene SIRT1 to extend lifespan in model organisms[19].
  • IGF1 Signaling Inhibitors: Spermidine supplements reduce insulin/IGF signaling to extend lifespan and healthspan in model organisms. In human clinical trials, acarbose lowers IGF1 levels in both men and women and significantly extends median lifespan in men[20].
  • mTOR Inhibitors: Rapamycin (a potent mTOR inhibitor) extends lifespan in mice and shows potential for treating multiple age-related diseases[21].
  • AMPK Activators: Metformin, aspirin, α-KG, and berberine (BBR) activate the AMPK pathway to improve healthspan in model organisms[22-23].
  • Stem Cell Anti-Aging Agents: Vitamin C alleviates premature stem cell senescence caused by WRN gene deficiency; WM-3835 (a bioactive molecule inhibitor) downregulates SASP gene expression to reduce stem cell inflammation; quercetin and gallic acid support skeletal muscle stem cell anti-aging; uridine rejuvenates aged human stem cells[24-25].
However, the molecular mechanisms by which these drugs/supplements intervene in aging remain unclear. Further clinical trials are needed to determine their indications, dosages, and administration timelines.

2. Gene Therapy

Gene therapy modifies nucleotide sequences at specific genomic loci (via addition, deletion, or alteration) using gene-editing technologies to alleviate aging phenotypes or extend healthspan[26]. Key approaches include:
  • In vivo gene therapy: Directly modify aging-related genes in senescent cells to reduce inflammation and prevent telomere shortening[27].
  • Transplantation of genetically engineered cells: Enhance stem cells via genetic modification to improve regenerative capacity and stress resistance, then transplant these cells to replace aged stem cells and counteract the aging microenvironment[28].
  • Elimination of abnormally accumulated senescent cells: Use gene-editing technologies to directly induce senescent cell apoptosis[29].

3. AI, Systems Biology, and Novel Technologies for Aging Research

With advances in computer science, artificial intelligence (AI) and systems biology are now used to identify universal aging hallmarks from multi-omics data (genomics, transcriptomics, proteomics, methylomics, metabolomics, microbiomics) and screen anti-aging drugs. Additionally, predictive models based on aging clocks and quantitative omics data have been developed to enable targeted interventions for delaying or reversing biological age[30].
Figure: Two Parallel and Synergistic Directions for AI- and Systems Biology-Aided Anti-Aging Drug Discovery
  • Left: Integrating multi-omics data (genomics, transcriptomics, proteomics, methylomics, microbiomics) and clinical data (blood tests, EEG/ECG, behavioral activity) to identify aging biomarkers;
  • Right: Using AI models (e.g., CNN-based DLEPS) to predict biological age and screen anti-aging drugs.
Other novel technologies supporting aging research include[31]:
  • Model systems: In vitro and in vivo models for aging studies;
  • Single-cell omics technologies: Single-cell genomics, transcriptomics, and proteomics;
  • Imaging-based technologies: Probes and in vivo imaging tools;
  • Computational methods: Algorithms for analyzing aging-related data.
Figure: Four Novel Technology Fields Supporting Aging Research

Part 4: Conclusion and Outlook

Thanks to collaborative research across disciplines, we now understand the complex mechanisms of aging and numerous intervention strategies. We have entered a golden era of aging research—aging can be prevented, delayed, and even reversed in some cases.
However, whether it is possible to extend human maximum lifespan remains an open question. Nevertheless, a large number of clinical trials on anti-aging interventions are underway, laying a solid foundation for lifespan extension.
We can remain optimistic and look forward to new discoveries in the field of aging biology. Due to space limitations, this article provides only a brief overview of aging mechanisms and interventions. For in-depth reading, the full review (with original translation) is available upon request.

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