Reversing cellular aging: a plan to test the approach in people

Nature reported that “partial reprogramming,” an experimental approach intended to reverse cellular aging, is planned to enter its first human trial in the second half of 2026. The report appeared in the April 9 issue of Nature Briefing; it does not mean that aging reversal or safety has been demonstrated in people. The materials provided do not establish whether the trial has since begun.

Partial reprogramming aims to reverse a cell’s aged state by inducing the expression of certain proteins. A key challenge is making this change safely while preserving cell function. The briefing explained that excessive reversal could cause cells to lose their function or become cancerous.

The briefing also described the possibility that this approach could lead to rejuvenation of entire organs or the whole body, but this was a prospect raised by some experts on the condition that safety is established. It is not a treatment outcome observed in people. The briefing did not specify the diseases to be studied, participant characteristics, administration method, comparator group, outcome measures, or follow-up period, making it difficult to assess the trial’s detailed design or anticipated benefits.

Noncoding DNA that affected sex development in mice

The same briefing covered a separate study in which modifying enhancer 13 (En13), a noncoding regulatory region on the X chromosome, altered sex development in female mouse embryos. Noncoding DNA comprises regions that do not encode proteins. This case shows that changes in a regulatory region within such DNA can affect reproductive organ development.

The researchers observed the formation of male genitalia and small testes following En13 modification. Both copies of En13 on the two X chromosomes had to be altered for this change to occur. So when reading the description “a change at one DNA site,” it is important to keep in mind that modification of En13 on both X chromosomes was required.

The formation of testes does not in itself indicate normal testicular function or reproductive capacity. The materials provided contain no results assessing these outcomes. En13 is also present in humans, but these materials cannot establish whether the changes observed in mice would also occur in people. The briefing cited a Nature Communications paper but did not include the scale of the experiments or detailed analytical results.

Genetic variants linked to individual differences in response to GLP-1 drugs

Another study on obesity treatments was described as finding that people with one or two copies of a particular variant in the gene encoding the GLP-1 receptor lost more weight during treatment than people without the variant. GLP-1 is a hormone whose action is mimicked by several obesity drugs. Two other variants near the receptor gene were associated with an increased likelihood of drug-related nausea and vomiting.

These findings offer genetic clues that could help explain why weight-loss effects and side effects vary from person to person. However, observing an association alone does not show that genes determine treatment response. The briefing did not specify the drugs studied, participant numbers or characteristics, treatment duration, or the size of the difference in weight loss. It is therefore not possible to assess how much these variants explain individual differences or whether prescribing based on genetic testing improves treatment outcomes.

These three topics are not findings from a single study; the news report brings together a planned human trial and separate studies. The evidence level and scope of what has been established should be considered separately for each. For details, see the April 9, 2026 issue of Nature Briefing.