Rosa Rubicondior: Malevolent Design - If Scientists Can Do It, Why Couldn't Creationism's Putative Designer?

Experimental Drug Repairs DNA Damage Caused by Disease | Cedars-Sinai Newsroom

Researchers at Cedars-Sinai have developed a synthetic RNA molecule that can help repair DNA in damaged tissues such as the myocardium following a myocardial infarction (MI). Their research is the basis for a paper just published in Science Translational Medicine

This raises a troubling question for ID creationists: if scientists can do it, why couldn’t their putative omniscient, omnipotent and, above all, omnibenevolent designer god do it? There are only a limited number of possibilities if we grant the ID proponents their designer god for the sake of argument:

It lacks the ability — in other words, it isn’t omnipotent.
It didn’t know it would be needed — in other words, it isn’t omniscient.
It doesn’t care — in other words, it isn’t omnibenevolent.
It doesn’t want us to repair damaged DNA so we continue to suffer the consequences — in other words, it is malevolent.

This is, of course, just another example of science discovering something that any intelligent, benevolent designer would have anticipated and provided, if such an entity had really designed us.

So, apart from those explanations — none of which flatter their putative designer — the only option left to creationists is that the absence of this DNA repair mechanism is the result of an unintelligent natural process in which their supposed designer played no part, such as evolution.

Unfortunately for them, creationists would have to abandon creationism and admit to being wrong if they accepted the naturalistic explanation. Sadly for them, creationists don’t see admitting being wrong as the intellectually honest thing to do, but as a sign of weakness and giving in to scientists and the physical evidence all ganging up to test their resolve.

This should trouble any creationist who understands the implications, so their cult leaders need to work hard to ensure none of their followers know about these things or develop the intellectual sophistication to appreciate the consequences.

What the Researchers Did — in Plain English.

Scientists at Cedars-Sinai developed a synthetic RNA molecule — they call it **TY1**— inspired by a naturally occurring human RNA. [1]
TY1 works by boosting the activity of a gene called TREX1. TREX1 is an “exonuclease” — an enzyme that helps clean up damaged or misplaced DNA fragments inside cells. [1]
In animal experiments (specifically in models of heart attack, or Myocardial Infarction, MI), treatment with TY1 led to smaller scars in the heart. That suggests the heart tissue healed better than it otherwise would — presumably because damaged DNA was cleared out and repaired. [1]
Importantly, the beneficial effects depended on immune cells called macrophages. When those macrophages were removed, the drug no longer worked. On the other hand, giving macrophages that had been exposed to TY1 (or forced to produce more TREX1) to other animals reproduced the protective effect. That shows the drug works via influencing these immune cells. [1]
The scientists propose that TY1 represents the first of a new class of medicines — which they dub “exomers”— aimed at repairing tissue damage by enhancing the body’s own DNA-cleanup and repair machinery rather than by replacing cells (e.g. via stem-cell therapy). [2]
Because DNA damage is implicated in many conditions — not just heart-attack scars, but also chronic inflammation, autoimmune disease, and maybe organ damage from injury or disease — TY1 (or future exomer-drugs) could potentially be used to treat a wide variety of diseases. [3]
In short: the researchers discovered an RNA-based therapy that helps the body clear damaged DNA and heal tissues — a new way of encouraging recovery after serious injury or disease.

Glossary — What the Key Terms Mean

Term Meaning (in this context)

RNA (ribonucleic acid) A type of molecule in cells, similar to DNA, but usually used to carry messages (instructions) from genes or to play regulatory roles. Not all RNA codes for proteins; some RNAs have other roles — “non-coding RNAs.”

Non-coding RNA (ncRNA) RNA molecules that don’t code for proteins, but can regulate gene expression or other cellular processes. TY1 is an engineered non-coding RNA. [1]

Exonuclease An enzyme that cuts away unwanted or damaged pieces of DNA (or RNA) — a kind of molecular “cleanup crew.” In this case, TREX1 is the exonuclease. [1]

Macrophage A type of immune cell that among other things can clean up debris and damaged material in tissues — important for repair and healing. In this study, macrophages play a critical role in tissue recovery when TY1 is used. [1]

Scarring (fibrosis) After tissue damage (like a heart attack), the body often patches the damage with scar tissue — which is functional but weaker than original tissue. Reducing scarring means better recovery and stronger function..

Exomer The term the researchers use for this new class of drugs (like TY1) — synthetic non-coding RNAs designed to trigger the body’s own repair systems (via DNA cleanup and regeneration), rather than replacing cells. [2]

Tissue regeneration / repair The process where the body restores damaged tissue to healthier state — ideally with native tissue rather than scar or damaged tissue.

Glossary — What the Key Terms Mean
Term	Meaning (in this context)
RNA (ribonucleic acid)	A type of molecule in cells, similar to DNA, but usually used to carry messages (instructions) from genes or to play regulatory roles. Not all RNA codes for proteins; some RNAs have other roles — “non-coding RNAs.”
Non-coding RNA (ncRNA)	RNA molecules that don’t code for proteins, but can regulate gene expression or other cellular processes. TY1 is an engineered non-coding RNA. [1]
Exonuclease	An enzyme that cuts away unwanted or damaged pieces of DNA (or RNA) — a kind of molecular “cleanup crew.” In this case, TREX1 is the exonuclease. [1]
Macrophage	A type of immune cell that among other things can clean up debris and damaged material in tissues — important for repair and healing. In this study, macrophages play a critical role in tissue recovery when TY1 is used. [1]
Scarring (fibrosis)	After tissue damage (like a heart attack), the body often patches the damage with scar tissue — which is functional but weaker than original tissue. Reducing scarring means better recovery and stronger function..
Exomer	The term the researchers use for this new class of drugs (like TY1) — synthetic non-coding RNAs designed to trigger the body’s own repair systems (via DNA cleanup and regeneration), rather than replacing cells. [2]
Tissue regeneration / repair	The process where the body restores damaged tissue to healthier state — ideally with native tissue rather than scar or damaged tissue.

But for those who aren’t afraid of scientific evidence because it doesn’t threaten them and make them feel weak, the findings of the Cedars-Sinai group are summarised in a news item by Stephanie Cajigal.

Experimental Drug Repairs DNA Damage Caused by Disease
Novel Molecule Engineered in Lab Is Prototype for a New Class of Powerful Drugs, Cedars-Sinai Researchers Say
Cedars-Sinai scientists have developed an experimental drug that repairs DNA and serves as a prototype for a new class of medications that fix tissue damage caused by heart attack, inflammatory disease or other conditions.

Investigators describe the workings of the drug, called TY1, in a paper published in Science Translational Medicine.

By probing the mechanisms of stem cell therapy, we discovered a way to heal the body without using stem cells. TY1 is the first exomer—a new class of drugs that address tissue damage in unexpected ways.

Dr Eduardo Marbán, senior author
Cedars-Sinai Medical Center
Smidt Heart Institute
Los Angeles, CA USA.

TY1 is a laboratory-made version of an RNA molecule that naturally exists in the body. The research team was able to show that TY1 enhances the action of a gene called TREX1, which helps immune cells clear damaged DNA. In so doing, TY1 repairs damaged tissue.

The development of TY1 has been more than two decades in the making. It started when Marbán’s previous laboratory at Johns Hopkins University developed a technique to isolate progenitor cells from the human heart. Like stem cells, progenitor cells can turn into new healthy tissue, but in a more focused manner than stem cells. Heart progenitor cells promote the regeneration of the heart, for example.

Later, at Marbán’s lab at Cedars-Sinai, Ahmed Ibrahim, PhD, MPH, discovered that these heart progenitor cells send out tiny molecule-filled sacs called exosomes. These sacs are loaded with RNA molecules that help repair and regenerate injured tissue.

Exosomes are like envelopes with important information. We wanted to take apart these coded messages and figure out which molecules were, themselves, therapeutic.

Professor Ahmed Gamel-Eldin Ibrahim, first author of the paper.
Cedars-Sinai Medical Center
Smidt Heart Institute
Los Angeles, CA USA.

Scientists genetically sequenced the RNA material inside the exosomes. They found that one RNA molecule was more abundant than the others, hinting it might be involved in tissue healing. The investigators found the natural RNA molecule to be effective in promoting healing after heart attacks in laboratory animals. TY1 is the synthetic, engineered version of that RNA molecule, designed to mimic the structure of approved RNA drugs already in the clinic. TY1 works by increasing the production of immune cells that reverse DNA damage, a process that minimizes the formation of scar tissue after a heart attack.

By enhancing DNA repair, we can heal tissue damage that occurs during a heart attack. We are particularly excited because TY1 also works in other conditions, including autoimmune diseases that cause the body to mistakenly attack healthy tissue. This is an entirely new mechanism for tissue healing, opening up new options for a variety of disorders.

Professor Ahme d Gamel-Eldin Ibrahim, first author of the paper.
Cedars-Sinai Medical Center
Smidt Heart Institute
Los Angeles, CA USA.

The investigators next plan to study TY1 in clinical trials.

Other Cedars-Sinai authors include Alessandra Ciullo, Hiroaki Komuro, Kazutaka Miyamoto, Xaviar M. Jones, Shukuro Yamaguchi, Kara Tsi, Jessica Anderson, Joshua Godoy Coto, Diana Kitka, Ke Liao, Chang Li, Alice Rannou, Asma Nawaz, Ashley Morris, Cristina H. Marbán, Jamie Lee, Nancy Manriquez, Yeojin Hong, Arati Naveen Kumar, James F. Dawkins, and Russell G. Rogers.

Publication:
Ahmed Gamal-Eldin Ibrahim et al.
Augmentation of DNA exonuclease TREX1 in macrophages as a therapy for cardiac ischemic injury. Sci. Transl. Med. 17, eadp1338 (2025). DOI:10.1126/scitranslmed.adp1338

Abstract
Noncoding RNAs (ncRNAs) are increasingly recognized as promising therapeutic candidates. Here, we report the development of therapeutic Y RNA 1 (TY1), a synthetic ncRNA bioinspired by a naturally occurring human small Y RNA with immunomodulatory properties. TY1 up-regulates three-prime DNA exonuclease 1 (TREX1), an exonuclease that rapidly degrades cytosolic DNA. In preclinical models of myocardial infarction (MI) induced by ischemia-reperfusion, TY1 reduced scar size. The cardioprotective effect of TY1 was abrogated by prior depletion of macrophages and mimicked by adoptive transfer of macrophages exposed to either TY1 or Trex1 overexpression. Inhibition of Trex1 in macrophages blocked TY1 cardioprotection. Consistent with a central role for Trex1, TY1 attenuated DNA damage in the post-MI heart. The key beneficial effects appear to be mediated by extracellular vesicles secreted by TY1-conditioned macrophages. This previously undescribed mechanism—pharmacological up-regulation of Trex1 in macrophages—establishes TY1 as the prototype for a new class of ncRNA drugs with disease-modifying bioactivity. We refer to this potential new class of ncRNA drugs as exomers because of the identification of their parent molecules in extracellular vesicles.

Ahmed Gamal-Eldin Ibrahim et al.
Augmentation of DNA exonuclease TREX1 in macrophages as a therapy for cardiac ischemic injury. Sci. Transl. Med. 17, eadp1338 (2025). DOI:10.1126/scitranslmed.adp1338

© 2025 The American Association for the Advancement of Science.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

The more we learn about biology, the more striking the contrast becomes between what creationists claim about their supposed designer and what the evidence actually shows. If life were the product of an all-knowing, all-powerful and benevolent intelligence, then discoveries like this should not be revelations at all — they ought to be features we already possess. Instead, scientists repeatedly uncover mechanisms that any competent designer would have incorporated from the outset but which evolution, driven by incremental change and historical constraint, could not easily produce.

This widening gap leaves creationism with no coherent explanation. Either their designer lacked foresight, lacked ability, or lacked compassion — or it simply wasn’t involved. None of these options fit the attributes creationists insist upon. What does fit the evidence is the naturalistic picture: living organisms are the products of unguided evolutionary processes that optimise only for survival and reproduction, not for efficiency, longevity, or resilience.

As science continues to reveal how much better our bodies could function, and how many flaws can be traced to evolutionary compromises rather than deliberate planning, the creationist narrative becomes ever more untenable. Their movement’s leaders are therefore compelled to shield followers from these developments, because the more clearly we understand how biology works — and how it could work better — the harder it becomes to maintain the illusion of intentional design.

Ultimately, these advances do not merely improve medicine; they also expose the intellectual bankruptcy of creationism. Every new discovery of a repair mechanism we lack, but could easily imagine in a genuinely designed organism, underscores the same conclusion: nature is not the product of a perfect mind, but of a long, messy, and entirely natural evolutionary history.

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